Influence of various factors on the human cardiovascular system. Presentation on the topic "The influence of factors on the cardiovascular system" Environmental factors affecting the circulatory system

The principle of blood movement. The third principle of hydrodynamics, applied to blood flow, reflects the law of conservation of energy and is expressed in the fact that the energy of a certain volume of flowing fluid, which is a constant value, consists of: a) potential energy (hydrostatic pressure), representing the mass of the blood column; b) potential energy (static pressure) under pressure on the wall; c) kinetic energy (dynamic pressure) of the moving blood flow after cardiac output. The addition of all types of energy gives the total pressure and is a constant value. Therefore, taking into account the law of conservation of energy, we see that when the blood vessel narrows, the blood flow velocity increases, and the potential energy decreases. In this case, the wall stress is very small. Conversely, when blood flow slows down in the dilated vessels (sinusoids), the energy of the moving flow decreases and the potential energy (pressure on the vessel wall) increases.

Regulation of the activity of the cardiovascular system. Neurohumoral self-regulation. Constant pressure is maintained in the arterial system; it can only temporarily change due to a change in the functional state of a person (labor processes, sports exercises, sleep). Level Consistency blood pressure in the arteries is provided by mechanisms of self-regulation. In the wall of the aortic arch and carotid sinus (the area of ​​branching of the common carotid artery into internal and external), there are pressoreceptors, i.e., receptors that are sensitive to pressure changes. With each systole of the heart, blood pressure in the arteries rises, and during diastole and outflow of blood to the periphery, it decreases. Pulse pressure fluctuations excite pressoreceptors, and along the sensitive (afferent) fibers, bursts of impulses arising in them are conducted to the central nervous system to the centers of cardiac inhibition and the vasomotor center, maintaining a constant state of excitation in them, called the tone of the centers.

With an increase in pressure in the aorta and carotid artery, impulses become more frequent, a continuous, so-called threatening, impulse may occur, which increases the tone of the center of the vagus nerve and inhibits the vasoconstrictor center. From the center of cardiac inhibition, impulses along the vagus nerves go to the heart and inhibit its activity. Inhibition of the vasoconstrictor center leads to a decrease in vascular tone and they expand. Blood pressure reaches the initial level - normalizes. Thus, with the participation of the mechanism of self-regulation in animals and humans, normal level blood pressure, which provides the necessary blood supply to the tissues.

Humoral regulation. Changes in the content of various substances in the blood also affect the cardiovascular system. So, the work of the heart is reflected in the change in the blood level of potassium and calcium. Increasing the calcium content increases the frequency and strength of contractions, increases the excitability and conduction of the heart. Potassium does the opposite. During emotional states: anger, fear, joy - adrenaline enters the blood from the adrenal glands. It has the same effect on the cardiovascular system as irritation of the sympathetic nerves: it increases the work of the heart and constricts the blood vessels, while the pressure rises. This is how the hormone works. thyroid gland thyroxine. The pituitary hormone vasopressin constricts arterioles. It has now been established that vasodilators are formed in many tissues. Vasoconstrictor substances include adrenaline, noradrenaline, vasopressin (hormone of the posterior pituitary gland), serotonin (formed in the brain and intestinal mucosa). Vasodilation is caused by metabolites - carbonic and lactic acids and the mediator acetylcholine. Expands arterioles and increases the filling of capillaries histamine, which is formed in the walls of the stomach and intestines, in the skin when it is irritated, in working muscles.

Blood pressure. An indispensable condition for the movement of blood through the system of blood vessels is the difference in blood pressure in the arteries and veins, which is created and maintained by the heart. With each systole of the heart, a certain volume of blood is pumped into the arteries. Due to the high resistance in the arterioles and capillaries, until the next systole, only part of the blood has time to pass into the veins and the pressure in the arteries does not drop to zero.

arteries. Obviously, the level of pressure in the arteries should be determined by the value of the systolic volume of the heart and the resistance in the peripheral vessels: the more forcefully the heart contracts and the more narrowed the arterioles and capillaries, the higher the blood pressure. In addition to these two factors: the work of the heart and peripheral resistance, the volume of circulating blood and its viscosity affect the magnitude of blood pressure.

As you know, severe bleeding, namely the loss of up to 1/3 of the blood, leads to death from the non-return of blood to the heart. The viscosity of the blood increases with debilitating diarrhea or heavy sweating. This increases peripheral resistance and requires higher blood pressure to move blood. The work of the heart increases, blood pressure rises.

Under normal conditions, the walls of the arteries are stretched and are in a state of elastic tension. When during systole the heart ejects blood into the arteries, then only part of the heart's energy is spent on moving the blood, a significant part goes into the energy of the elastic tension of the walls of the arteries. During diastole, the stretched elastic walls of the aorta and large arteries put pressure on the blood and therefore the flow of blood does not stop.

In the arterial system, due to the rhythmic work of the heart, blood pressure periodically fluctuates: it rises during ventricular systole and decreases during diastole, as blood flows to the periphery. highest pressure, observed during systole, is called the maximum, or systolic, pressure. The lowest pressure during diastole is called minimum, or diastolic. The amount of pressure depends on age. In children, the walls of the arteries are more elastic, so their pressure is lower than in adults. In healthy adults, the maximum pressure is normally 110-120 mm Hg. Art., and the minimum 70-80 mm Hg. Art. By old age, when the elasticity of the vascular walls decreases as a result of sclerotic changes, the level of blood pressure rises.

The difference between the maximum and minimum pressure is called pulse pressure. It is equal to 40-50 mm Hg. Art.

The value of blood pressure is an important characteristic of the activity of the cardiovascular system.

capillaries. Due to the fact that the blood in the capillaries is under pressure, in the arterial part of the capillaries, water and substances dissolved in it are filtered into the interstitial fluid. At its venous end, where blood pressure decreases, the osmotic pressure of plasma proteins sucks the interstitial fluid back into the capillaries. Thus, the flow of water and substances dissolved in it, in the initial part of the capillary goes out, and in its final part - inside. In addition to the processes of filtration and osmosis, the diffusion process also participates in the exchange, i.e., the movement of molecules from a medium with a high concentration to an environment where the concentration is lower. Glucose and amino acids diffuse from the blood into tissues, while ammonia and urea diffuse in the opposite direction. However, the capillary wall is a living semi-permeable membrane. The movement of particles through it cannot be explained only by the processes of filtration, osmosis, and diffusion.

The permeability of the capillary wall is different in different bodies and selective, i.e., some substances pass through the wall and others are retained. Slow blood flow in the capillaries (0.5 mm/s) contributes to the flow of metabolic processes in them.

Vienna unlike arteries, they have thin walls with a poorly developed muscular membrane and a small amount of elastic tissue. As a result, they are easily stretched and easily squeezed. In the vertical position of the body, the return of blood to the heart is prevented by gravity, so the movement of blood through the veins is somewhat difficult. For him, one pressure created by the heart is not enough. Residual blood pressure even at the beginning of the veins - in the venules is only 10-15 mm Hg. Art.

Basically, three factors contribute to the movement of blood through the veins: the presence of valves in the veins, contractions of nearby skeletal muscles, and negative pressure in the chest cavity.

Valves are present mainly in the veins of the extremities. They are located so that they pass blood to the heart and prevent its movement in the opposite direction. The contracting skeletal muscles press on the pliable walls of the veins and move blood towards the heart. Therefore, movements contribute to venous outflow, increasing it, and prolonged standing causes stagnation of blood in the veins and expansion of the latter. In the chest cavity, the pressure is below atmospheric, i.e., negative, and in abdominal cavity positive. This pressure difference is responsible for the suction action. chest which also promotes the movement of blood through the veins.

Pressure in arterioles, capillaries and veins. As blood moves through the bloodstream, the pressure decreases. The energy generated by the heart is spent on overcoming the resistance to blood flow that occurs due to the friction of blood particles against the wall of the vessel and against each other. Different parts of the bloodstream have different resistance to blood flow, so the pressure decrease is uneven. The greater the resistance of this section, the more sharply the pressure level drops in it. The areas with the greatest resistance are arterioles and capillaries: 85% of the heart's energy is spent on moving blood through arterioles and capillaries, and only 15% is spent on moving it through large and medium arteries and veins. The pressure in the aorta and large vessels is 110-120 mm Hg. Art., in arterioles - 60-70, at the beginning of the capillary, at its arterial end - 30, and at the venous end - 15 mm Hg. Art. In the veins, the pressure decreases gradually. In the veins of the extremities, it is 5-8 mm Hg. Art., and in large veins near the heart it can even be negative, that is, a few millimeters of mercury below atmospheric.

Distribution curve of blood pressure in the vascular system. 1 - aorta; 2, 3 - large and medium arteries; 4, 5 - terminal arteries and arterioles; 6 - capillaries; 7 - venules; 8-11 - final, middle, large and hollow veins

Blood pressure measurement. The value of blood pressure can be measured by two methods - direct and indirect. When measuring in a direct, or bloody, way, a glass cannula is tied into the central end of the artery or a hollow needle is inserted, which is connected with a rubber tube to a measuring device, such as a mercury manometer. In a direct way, the pressure in a person is recorded during major operations, for example, on the heart, when it is necessary to continuously monitor the level of pressure.

To determine the pressure by an indirect, or indirect, method, the external pressure is found that is sufficient to occlude the artery. In medical practice, blood pressure in the brachial artery is usually measured by the Korotkoff indirect sound method using a Riva-Rocci mercury sphygmomanometer or a spring tonometer. A hollow rubber cuff is placed on the shoulder, which is connected to an injection rubber bulb and a pressure gauge showing the pressure in the cuff. When air is forced into the cuff, it presses on the tissues of the shoulder and compresses the brachial artery, and the pressure gauge shows the value of this pressure. Vascular tones are heard with a phonendoscope above the ulnar artery, below the cuff. N. S. Korotkov found that in an uncompressed artery there are no sounds during the movement of blood. If the pressure is raised above the systolic level, then the cuff completely occludes the lumen of the artery and the blood flow in it will stop. There are also no sounds. If we now gradually release air from the cuff and reduce the pressure in it, then at the moment when it becomes slightly lower than systolic, the blood during systole will break through the squeezed area with great force and a vascular tone will be heard below the cuff in the ulnar artery. The pressure in the cuff at which the first vascular sounds appear corresponds to the maximum, or systolic, pressure. With further release of air from the cuff, i.e., a decrease in pressure in it, the tones increase, and then either sharply weaken or disappear. This moment corresponds to diastolic pressure.

Pulse. The pulse is called the rhythmic fluctuations in the diameter of arterial vessels that occur during the work of the heart. At the moment of expulsion of blood from the heart, the pressure in the aorta rises, and the wave high blood pressure extends along the arteries to the capillaries. It is easy to feel the pulsation of the arteries that lie on the bone (radial, superficial temporal, dorsal artery of the foot, etc.). Most often examine the pulse on the radial artery. Feeling and counting the pulse, you can determine the heart rate, their strength, as well as the degree of elasticity of the vessels. An experienced doctor, by pressing on the artery until the pulsation stops completely, can quite accurately determine the height of blood pressure. In a healthy person, the pulse is rhythmic, i.e. strikes follow at regular intervals. In diseases of the heart, rhythm disturbances - arrhythmia - can be observed. In addition, such characteristics of the pulse as tension (pressure in the vessels), filling (amount of blood in the bloodstream) are also taken into account.

In large veins near the heart, pulsation can also be observed. The origin of the venous pulse is diametrically opposed to that of the arterial pulse. The outflow of blood from the veins to the heart stops during atrial systole and during ventricular systole. These periodic delays in the outflow of blood cause the veins to overflow, stretch their thin walls and cause them to pulsate. The venous pulse is examined in the supraclavicular fossa.

In the conditions of a modern city, a person is exposed to a wide range of environmental social and environmental factors which largely determine adverse changes in the state of his health.

Age, gender and individual characteristics of a person determine the boundaries of his functional capabilities, the degree of adaptation of the body to environmental conditions, its physical and social influences, and this characterizes the level of his health. From this point of view, the disease is the result of exhaustion and breakdown of adaptive mechanisms, when the resistance to adverse effects is sharply reduced. The functional capabilities of the body, which determine the degree of realization of vital biological and social needs, constitute the so-called adaptive potential.

Pollution of the natural environment affects the physical and mental health of a person, his vitality, labor productivity.

The adaptive adaptive capabilities of a person are not always sufficient for the normal functioning of the body in a new ecological environment, which leads to serious consequences. The reaction of the human body to the influence of new negative environmental factors should be considered the emergence of previously unknown medical diseases, as well as an increase in the prevalence and severity of many forms of pathology. This is especially evident in living conditions in large cities with developed industry. Recorded here:

chemical pollution of air, water, land, food products;

acoustic discomfort;

artificial use of low-quality building materials and other shortcomings of urban planning;

harmful energy radiation;

geopathogenic zones, etc.

According to the classification of V.V. Khudoleya, S.V. Zubarev and O.T. Dyatlechenko, the main changes in all health indicators, characteristic of the modern period of development of our country, include:

accelerating the pace of changes in all health indicators;

formation of a new, non-epidemic type of pathology;

the acceleration of demographic change, expressed in the aging of the population;

an increase in the incidence of diseases of the circulatory system, chronic non-specific diseases of the respiratory system;

a sharp increase in the proportion of endocrine, allergic, birth defects development, diseases of the immune system, as well as some infectious diseases;

development of multiple pathologies.

A significant part of the population is now in a state where the disease has not yet manifested itself, but general malaise is becoming a common background condition. The most severe consequences for the health of urban residents are brought by the chronic impact of degenerative changes in the external environment of cities. Chemicals circulating in the environment enter the human body in relatively small quantities, therefore, with a low intensity of their exposure, as a rule, there is no rapid onset of clearly pronounced pathological changes. Morbidity and even more so mortality in such cases is last stage the process of intoxication of the body with harmful substances.

The relationship between the level of impact on a person of limiting factors and the state of health (in particular, the level of morbidity) is non-linear. So, for example, at a low level of chemical pollution of the environment, activation of the protective reserves of the body is observed - stimulation of neutralization. These processes occurring in the human body are weakly manifested in terms of morbidity. An increase in the level of chemical exposure is accompanied by inhibition of the processes of excretion from the body and neutralization of xenobiotics. A further increase in the level of environmental pollution leads to a sharp increase in the number of cases of manifestation of pathologies in the population. As the impact of pollutants increases, adaptation mechanisms are activated that stabilize the level of morbidity. Further, the mechanisms of adaptation are disrupted, which leads to another rise in the level of morbidity in the population (Fig. 1). It should be borne in mind that the presented scheme of the dependence of morbidity on the ecological state of the environment is very simplified, since the causative factors of human disease are extremely numerous and affect a person in various combinations with each other.

Rice. Fig. 1. A simplified diagram of the dynamics of the incidence of the population (solid line) with an increase in the dose load of pollutants (dotted line) (according to: Kiselev, Fridman, 1997)

The pathological process is a complete manifestation of the impact of adverse environmental factors on the human body, its functions. Signs pathological process in the body along with the presence of acute or chronic disease are also changes in physiological functions (for example, pulmonary ventilation, functions of the central nervous system, blood oxidation), subjective symptomatology of various kinds, changes in internal comfort. Therefore, the chronic impact of environmental pollutants on the health of the population at first manifests itself in the form functional disorders, changes in immunobiological reactivity, slowing down physical development, but in the future it can lead to severe long-term consequences, including genetic ones. Environmental pollution is not only etiological factor the appearance of certain pathological conditions of the body, it has a well-known provocative role in the occurrence of chronic nonspecific diseases, its influence aggravates the course and prognosis of these pathological conditions of the body.

It is believed that the incidence of the population in large cities up to 40% (and in areas near powerful sources of emissions - up to 60%) is associated with environmental pollution, while in small cities - no more than 10%. From the point of view of the health of citizens, air pollution plays a leading role, since through it human contacts with the environment are more intense and longer than through water and food. In addition, many chemicals affect the body more actively if they enter it through the respiratory system. Atmospheric precipitation, absorbing gaseous, liquid and solid components of polluted air, acquire a new chemical composition and physico-chemical properties.

Most of the studies are devoted to the study of the impact on the health of the urban population of individual components of the environment. Atmospheric pollution has been studied most fully. A statistically significant dependence of the incidence of the population on atmospheric air pollution has been established for bronchitis, pneumonia, emphysema (expansion of pulmonary vesicles - alveoli, leading to compression of small blood vessels and worsening of gas exchange processes), acute respiratory diseases. A significant effect of air pollution on the duration of diseases has been established.

The danger of air pollution for the human body is largely determined by the fact that even at low concentrations of pollutants, due to round-the-clock filtration of polluted air by the lungs, a significant intake of pollutants can occur. harmful substances into the body. In addition, in the lungs there is a direct contact of pollutants with blood, which then enters the systemic circulation, bypassing an important detoxification barrier - the liver. That is why poisons that enter the human body in the process of breathing often act 80-100 times stronger than if they enter through gastrointestinal tract. The degree of impact of polluted atmosphere on the human body depends on the age of people. The most sensitive are 3-6 year old children and the elderly over 60 years of age.

For the urban environment, nitrogen oxides are a typical pollutant. They are formed during the combustion of any type of fuel, and in cities, motor transport accounts for up to 75% of their total emissions. It is important to emphasize that even if there is no nitrogen in the fuel, during its combustion, nitrogen oxides are still formed due to the interaction of oxygen and atmospheric nitrogen. When a person inhales air containing nitrogen oxides, they interact with the moist surface of the respiratory organs and form nitric and nitrous acids, affecting alveolar tissue lungs. This leads to their swelling and reflex disorders. In the respiratory tract, they combine with tissue alkalis and form nitrates and nitrites. Violation of the respiratory system gradually but steadily leads to an increase in the load on the heart and blood vessels, which, ultimately, can cause death. This circumstance explains the clearly pronounced trend of a sharp increase in deaths among patients with the indicated nosological forms of diseases during a sharp rise in the concentration of toxic substances in the air. Many other air pollutants can also adversely affect the cardiovascular system. In particular, carbon monoxide causes tissue hypoxia, which, in turn, contributes to the occurrence of negative shifts in the cardiovascular system.

Formed as a result of inhalation of air containing nitric oxide, nitrites and nitrates adversely affect the activity of almost all enzymes, hormones and other proteins that regulate metabolism, growth, development, and reproduction of the body. At a nitrogen dioxide concentration of less than 205 μg / m 3, a person experiences changes in cellular level. At a concentration of 205 to 512 μg / m 3, adaptive mechanisms are disrupted sensory systems, and at concentrations from 512 to 1025 µg/m 3 changes occur in the biochemical processes and structural organization of the lungs. Nitrogen dioxide concentrations in the range of 1025-3075 µg/m 3 cause an increase in resistance respiratory tract in patients with bronchial diseases, and in the range of 3075-5125 μg / m 3 - the same changes, but in healthy people.

Sulfur dioxide irritates the respiratory tract, leads to spasms of the bronchi, as a result of its interaction with the mucous membrane, sulfurous and sulfuric acids are formed. General action sulfur dioxide is manifested in the violation of carbohydrate and protein metabolism, inhibition of oxidative processes in the brain, liver, spleen, muscles. It irritates the hematopoietic organs, promotes the formation of methemoglobin, causes changes in the endocrine organs, bone tissue, disrupts the generative function of the body, embryotoxic and gonadotoxic effects.

Serious problems in the urban population occurs with an increase in the concentration of ozone in the surface air layer. It is a very powerful oxidizing agent, and its toxicity increases with increasing air temperature. Patients with asthma and allergic rhinitis (runny nose) are more sensitive to the effects of ozone.

The role of products of combustion of automobile fuel as environmental pollutants is great. In the exhaust gases of cars is, and in significant quantities, carbon monoxide - carbon monoxide. Carbon monoxide, binding in the blood with erythrocyte hemoglobin, turns into carboxyhemoglobin, which, unlike hemoglobin, does not have the ability to carry oxygen to body tissues.

Thus, tissue respiration worsens, having a negative impact on the activity of the cardiovascular system, the functional state of the central nervous system. Therefore, people in areas of high gas concentrations often show signs of chronic carbon monoxide poisoning: fast fatiguability, headaches, tinnitus, pain in the heart area.

Polynuclear aromatic hydrocarbons, substances with toxic properties, are widely distributed in the air surrounding citizens. The impact of these substances on the human body is often associated with the appearance of malignant neoplasms. This group includes benzo(a)pyrene, which is characterized by the most pronounced mutagenic and carcinogenic activity, although, according to experts from the International Agency for Research on Cancer, there is no direct evidence of its carcinogenicity to humans. Dioxins belong to the same group of substances. The main source of their emissions are cars running on gasoline with anti-caking additives, garbage incinerators and even conventional stoves. The source of dioxins are steel mills and pulp and paper mills, traces of dioxins are found in products formed with the participation of chlorine. They are transported in the atmosphere over long distances (mainly sorbed on solid particles) and therefore spread globally. It is believed that many organochlorine compounds (including dioxins) reduce the efficiency of the immune system. As a result, the likelihood increases viral diseases and the severity of their course increases, the processes of regeneration (healing) of tissues slow down, which is decisive in the aging of self-renewing tissues.

In general, it can be said that various chemicals polluting the atmosphere of cities are characterized by a certain uniformity of action on the human body. So, many of them irritate the mucous membranes, which leads to an increase in the number of inflammatory diseases of the respiratory system, ENT organs, and eyes. Even in small amounts, they weaken the protective properties of the human body, affecting its immunological reactivity, increase the incidence of the cardiovascular system and bronchial asthma. A positive relationship was found between the level of pollution of the atmospheric air of cities by them and the growth of diseases of a genetic nature, an increase in the number of malignant neoplasms, an increase in allergic diseases, and an increase in cases of metabolic disorders. Based on studies conducted in the Japanese city of Osako, the relationship between the level of atmospheric air pollution and the death rate of city residents is shown.

This relationship is especially pronounced with cardiovascular, respiratory diseases, chronic rheumatic heart disease.

A specific problem for the population of many cities is the consequences of chlorination of drinking water. When it is chlorinated, the transformation of organochlorine and phosphorus pesticides into substances that turn out to be 2 times more toxic than the original components is observed. Chemical contamination of drinking water primarily causes diseases of the digestive and excretory systems. These include gastritis, stomach ulcers, cholelithiasis and urolithiasis, nephritis. Thus, with a 3-5-fold increase in the content of chlorides and sulfates in water, the incidence of bile and urolithiasis increases, while there is an increase in vascular pathology. Water pollution with organic and inorganic industrial waste leads to damage to the liver, hematopoietic apparatus, to the deposition of calcium salts.

The problem of the impact of water pollution on human health is becoming increasingly important due to fundamental changes in the very nature of wastewater. Both industrial and domestic waste waters contain wastes of synthetic detergents, which are based on surfactants - detergents. Treatment facilities used at modern waterworks do not provide the necessary efficiency of water purification from surfactants, which is the reason for their appearance in drinking water. When detergents enter the gastrointestinal tract, the walls of the esophagus and stomach are damaged, thereby disturbing their permeability. Having a long-term chronic effect on the human body, these substances can cause a sharp deterioration in the course of many diseases of the internal organs.

The problem of water pollution and its consequences for the human body is closely related to the sanitary and hygienic state of the soil. Currently, in agriculture, mineral fertilizers and chemical plant protection products - pesticides are used in huge quantities. Organochlorine compounds belonging to the group of pesticides, such as DDT and hexochloran, are relatively stable in the external environment and can accumulate in the tissues and fat of animal organisms. High concentrations of DDT and its metabolites, affecting mainly parenchymal organs and the central nervous system, contribute to the development of cirrhosis, malignant tumors, and hypertension.

Among the environmental factors that adversely affect the health of the urban population, in addition to chemical and biological substances, one should also include pollutants of a physical nature: noise, vibration, electromagnetic oscillations, and radioactive radiation.

One of the most important physical types of environmental pollution is acoustic noise. Studies have established that in terms of the degree of harmfulness of exposure to noise, it ranks second after chemical pollution of the environment. Daily exposure to low noise worsens the state of health, reduces the sharpness of attention, contributes to the emergence of neurosis, disorders of the nervous system and loss of hearing acuity. Under the action of noise, there are shifts in metabolism in the nervous tissue, the development of hypoxia, and neurohumoral changes in the body. Noise can cause activation of the system of organs of internal secretion in the form of an increase in the content of activating hormones in the blood and an increase in metabolic processes, inhibition of natural immunity, which can contribute to the formation of pathological processes.

According to Australian researchers, noise in cities leads to a reduction in life by 8-12 years. It is believed that with an increase in the level of street noise to 50-60 dB SL, an increase in the number of cardiovascular diseases in the population occurs. City noise causes coronary heart disease, hypertension. In people living in a noisy area, high blood cholesterol is more common than in residents of quiet neighborhoods. The totality of all disorders and dysfunctions arising under the influence of industrial noise, received at the suggestion of E.Ts. Andreeva-Galanina and co-authors, the generalizing name is "noise disease".

Many problems also arise in connection with the impact on humans of man-made magnetic and electromagnetic fields. They adversely affect the nervous system, and the most significant role in response to this powerful anthropogenic factor is played by the cardiovascular and endocrine systems. Yu.A. Dumansky and co-authors (1975) found the effect of short waves on the cardiovascular system, characterized by a decrease in heart rate, vascular hypotension, and worsening of cardiac conduction.

Conducted in the late 1980s. studies by American epidemiologists have revealed a positive relationship between the level of man-made electromagnetic fields and the growth of a number of diseases in the population: leukemia, brain tumors, multiple sclerosis, oncological diseases. The nervous system is most sensitive to the effects of fields. Significantly depressed and the immune system, and therefore the course of the infectious process in the body is aggravated, the immune system begins to act against the normal tissue antigens of its own body.

Summarizing the analysis of the literature on the pathophysiological features of the impact on the body of various anthropogenic environmental factors, we can conclude that, on the one hand, each of them can selectively affect the functions of individual organs and systems of the body and, thus, have a specific effect. On the other hand, these factors also have a non-specific effect, primarily affecting the central and autonomic nervous system, and therefore there may be adverse changes in various bodies and systems.

As can be seen from the material presented above, the factors affecting the health of the population of urbanized territories include many physical and chemical features of the environment. However, this list would be incomplete without including social conditions. Of the latter, saturation with contacts and informational redundancy of the environment are of the greatest importance. The rapid development of mass communications, according to many researchers, has become the cause of ecopsychological stress. Overloading the psyche with a huge flow of contradictions, usually negative information, led to the development, in particular, of information stress. Prolonged stress causes a violation of the immune and genetic apparatus, causes many mental and somatic diseases, increased mortality.

The appearance of pathologies in certain organs and systems under the influence of negative anthropogenic environmental factors can become a direct cause of premature aging of the human body, and even death.

General mortality of the population and average life expectancy are the most important indicators reflecting public health in international practice. Over the past 15 years, Russia has seen a deterioration in almost all demographic indicators. The dynamics of average life expectancy and mortality in our country is very unfavorable. Today, the average life expectancy in Russia is less than in developed countries, where the 70-year milestone has long been overcome. In our country, this figure is 67.7 years.

In order to determine which factors determine life expectancy, one should get acquainted with the structure of morbidity and mortality of the population. The incidence of the population of Russia is mainly determined by five classes of diseases. They make up more than 2/3 of all diseases. The most common diseases of the respiratory system - more than 1/3 of all diseases. The second place is occupied by diseases of the nervous system and sensory organs. This is followed by diseases of the cardiovascular system, diseases of the digestive system, as well as accidents, injuries and poisoning. The number of viral diseases is also growing.

The structure of mortality in Russia has certain differences from other countries of the world. Both in developed countries and in Russia, most people die from cardiovascular diseases (currently this is the cause of death for almost 56% of Russians). At the same time, it should be noted that in our country, mortality from this cause for last years doubled and became epidemic. In second place among the causes of death are accidents, injuries and poisonings, suicides and murders. For example, more than 30 thousand people die on the roads every year, and about 60 thousand people die from suicide. Further among the causes of death are oncological diseases and respiratory diseases.

The quality of the environment, combined with lifestyle, is the cause of the disease in 77% of cases, and the cause of premature death in 55% of cases. However, in real life, a small percentage of the population is affected by these extreme manifestations (illness and death). In the bulk of the population living in conditions of varying degrees of environmental pollution, the so-called pre-pathological states are formed: physiological, biochemical and other changes in the body, or accumulation of certain pollutants in organs and tissues without visible signs of health impairment. Such "pollution" of the body over time, along with a decrease in the number of any non-renewing structures and a deterioration in the quality of regulation and mutual coordination of vital processes in the body, is one of the main causes of aging of the body, including premature aging. Premature aging refers to any partial or more general acceleration in the rate of aging that results in a person being ahead of the average level of aging in their age group.

From a socioeconomic and medical point of view, premature aging in combination with age-related diseases, which develop rapidly, lead to decrepitude and disability. The reduction of labor resources is directly dependent on the decline in the life potential of the population. Thus, the most essential need of modern society is the development of new medical preventive and therapeutic technologies aimed at significantly increasing the health potential and slowing down the aging process itself.

The chapter deals with blood circulation at various levels of physical activity, lack and excess of oxygen, low and high ambient temperatures, and changes in gravity.

PHYSICAL ACTIVITY

Work can be dynamic, when resistance is overcome at a certain distance, and static, with isometric muscle contraction.

Dynamic work

Physical stress causes immediate reactions various functional systems, including muscular, cardiovascular and respiratory. The severity of these reactions is determined by the adaptability of the body to physical stress and the severity of the work performed.

Heart rate. According to the nature of the change in heart rate, two forms of work can be distinguished: light, non-fatiguing work - with the achievement of a stationary state - and heavy, fatigue-causing work (Fig. 6-1).

Even after the end of the work, the heart rate changes depending on the voltage that has taken place. After light work, the heart rate returns to its original level within 3-5 minutes; after hard work, the recovery period is much longer - with extremely heavy loads, it can reach several hours.

With hard work, blood flow and metabolism in the working muscle increases by more than 20 times. The degree of changes in indicators of cardio- and hemodynamics during muscular activity depends on its power and physical fitness (adaptability) of the organism (Table 6-1).

Rice. 6-1.Changes in heart rate in individuals with average performance during light and heavy dynamic work of constant intensity

In persons trained for physical activity, myocardial hypertrophy occurs, capillary density and contractile characteristics of the myocardium increase.

The heart increases in size due to hypertrophy of cardiomyocytes. The weight of the heart in highly skilled athletes increases to 500 g (Fig. 6-2), the concentration of myoglobin in the myocardium increases, the heart cavities increase.

The density of capillaries per unit area in a trained heart increases significantly. Coronary blood flow and metabolic processes increase in accordance with the work of the heart.

Myocardial contractility (the maximum rate of increase in pressure and ejection fraction) is markedly increased in athletes due to the positive inotropic action of sympathetic nerves.

Table 6-1.Changes in physiological parameters during dynamic work of different power in people who do not go in for sports (top line) and in trained athletes (bottom line)

During exercise, cardiac output increases due to an increase in heart rate and stroke volume, and changes in these values ​​are purely individual. In healthy young people (with the exception of highly trained athletes), cardiac output rarely exceeds 25 l / min.

Regional blood flow. At physical activity regional blood flow changes significantly (Table 6-2). Increased blood flow in working muscles is associated not only with an increase in cardiac output and blood pressure, but also with the redistribution of BCC. With maximum dynamic work, blood flow in the muscles increases by 18-20 times, in the coronary vessels of the heart by 4-5 times, but decreases in the kidneys and abdominal organs.

In athletes, the end-diastolic volume of the heart naturally increases (3-4 times more than the stroke volume). For an ordinary person, this figure is only 2 times higher.

Rice. 6-2.Normal heart and athlete's heart. An increase in the size of the heart is associated with elongation and thickening of individual myocardial cells. In the heart of a grown man for every muscle cell there is approximately one capillary

Table 6-2.Cardiac output and organ blood flow in humans at rest and during exercise of varying intensity

With muscle activity, myocardial excitability increases, the bioelectric activity of the heart changes, which is accompanied by a shortening of the PQ, QT intervals of the electrocardiogram. The greater the power of work and the lower the level of physical fitness of the body, the more the electrocardiogram parameters change.

With an increase in heart rate up to 200 per minute, the duration of diastole decreases to 0.10-0.11 s, i.e. more than 5 times in relation to this value at rest. The filling of the ventricles in this case occurs within 0.05-0.08 s.

Arterial pressure in humans during muscular activity increases significantly. When running, causing an increase in heart rate up to 170-180 per minute, the following increases:

Systolic pressure on average from 130 to 250 mm Hg;

Average pressure - from 99 to 167 mm Hg;

Diastolic - from 78 to 100 mm Hg.

With intense and prolonged muscular activity, the stiffness of the main arteries increases due to the strengthening of the elastic framework and the increase in the tone of smooth muscle fibers. In the arteries of the muscular type, moderate hypertrophy of the muscle fibers can be observed.

The pressure in the central veins during muscular activity, as well as the central blood volume, increases. This is due to an increase in venous blood return with an increase in the tone of the walls of the veins. The working muscles act as an additional pump, which is referred to as the "muscle pump", providing an increased (adequate) blood flow to the right heart.

The total peripheral vascular resistance during dynamic work can decrease by 3-4 times compared with the initial, non-working state.

Oxygen consumption increases by an amount that depends on the load and the efficiency of the efforts expended.

With light work, a steady state is reached, when oxygen consumption and its utilization are equivalent, but this occurs only after 3-5 minutes, during which the blood flow and metabolism in the muscle adapt to the new requirements. Until a steady state is reached, the muscle depends on a small oxygen reserve,

which is provided by O 2 associated with myoglobin, and from the ability to extract oxygen from the blood.

With heavy muscular work, even if it is performed with constant effort, a stationary state does not occur; like heart rate, oxygen consumption is constantly increasing, reaching a maximum.

oxygen debt. With the start of work, the need for energy increases instantly, but it takes some time for blood flow and aerobic metabolism to adjust; Thus, there is an oxygen debt:

In light work, the oxygen debt remains constant after reaching a steady state;

With hard work, it grows until the very end of the work;

At the end of work, especially in the first minutes, the rate of oxygen consumption remains above the level of rest - there is a "payment" of oxygen debt.

A measure of physical stress. As the intensity of dynamic work increases, the heart rate increases, and the rate of oxygen consumption increases; the greater the load on the body, the greater this increase compared to the level at rest. Thus, heart rate and oxygen consumption serve as a measure of physical stress.

Ultimately, the adaptation of the organism to the action of high physical loads leads to an increase in the power and functional reserves of the cardiovascular system, since it is this system that limits the duration and intensity of the dynamic load.

HYPODYNAMIC

The release of a person from physical labor leads to physical detraining of the body, in particular, to a change in blood circulation. In such a situation, one would expect an increase in efficiency and a decrease in the intensity of the functions of the cardiovascular system. However, this does not happen - the economy, power and efficiency of blood circulation are reduced.

IN big circle blood circulation often observe a decrease in systolic, mean and pulse blood pressure. In the pulmonary circulation, when hypokinesia is combined with a decrease in hydrostatic blood pressure (bed rest, weightless

bridge) increases blood flow to the lungs, increases pressure in the pulmonary artery.

At rest with hypokinesia:

Heart rate naturally increases;

Cardiac output and BCC decrease;

With prolonged bed rest, the size of the heart, the volume of its cavities, as well as the mass of the myocardium noticeably decrease.

The transition from hypokinesia to normal activity mode causes:

Pronounced increase in heart rate;

Increase in the minute volume of blood flow - IOC;

Decreased total peripheral resistance.

With the transition to intense muscular work, the functional reserves of the cardiovascular system decrease:

In response to a muscle load of even low intensity, the heart rate rapidly increases;

Shifts in blood circulation are achieved by including its less economical components;

At the same time, the IOC increases mainly due to an increase in heart rate.

Under conditions of hypokinesia, the phase structure of the cardiac cycle changes:

The phase of expulsion of blood and mechanical systole is reduced;

The duration of the phase of tension, isometric contraction and relaxation of the myocardium increases;

The initial rate of increase in intraventricular pressure decreases.

Myocardial hypodynamia. All of the above indicates the development of the phase syndrome of myocardial hypodynamia. This syndrome, as a rule, is observed in a healthy person against the background of a reduced return of blood to the heart during light physical exertion.

ECG changes.With hypokinesia, the electrocardiogram parameters change, which are expressed in positional changes, a relative slowdown in conduction, a decrease in the P and T waves, a change in the ratio of T values ​​in various leads, a periodic shift segment S-T, changing the process of repolarization. Hypokinetic changes in the electrocardiogram, regardless of the picture and severity, are always reversible.

Changes in the vascular system. With hypokinesia, a stable adaptation of the vascular system and regional blood flow to these conditions develops (Table 6-3).

Table 6-3.The main indicators of the cardiovascular system in humans under conditions of hypokinesia

Changes in the regulation of blood circulation. With hypokinesia, signs of the predominance of sympathetic influences over parasympathetic ones change the system of regulation of the activity of the heart:

The high activity of the hormonal link of the sympathoadrenal system indicates a high stress level of hypokinesia;

Increased excretion of catecholamines in the urine and their low content in tissues is realized by a violation of the hormonal regulation of the activity of cell membranes, in particular, cardiomyocytes.

Thus, the decrease in the functionality of the cardiovascular system during hypokinesia is determined by the duration of the latter and the degree of limitation of mobility.

CIRCULATION IN OXYGEN DEFICIENCY

As altitude increases, atmospheric pressure decreases, and the partial pressure of oxygen (PO 2 ) decreases in proportion to the decrease in atmospheric pressure. The reaction of the body (primarily the respiratory, circulatory and blood organs) to oxygen deficiency depends on its severity and duration.

For short-term reactions in high altitude conditions, only a few hours are required, for primary adaptation - several days and even months, and the stage of stable adaptation of migrants is acquired over the years. The most effective adaptive reactions are manifested in the indigenous population of high-mountain regions due to long-term natural adaptation.

Initial adaptation period

The movement of a person (migration) from the flat terrain to the mountains is accompanied by a pronounced change in the hemodynamics of the systemic and pulmonary circulation.

Tachycardia develops and the minute volume of blood flow (MOV) increases. Heart rate at an altitude of 6000 m in new arrivals at rest reaches 120 per minute. Physical activity causes more pronounced tachycardia and an increase in cardiac output than at sea level.

The stroke volume changes slightly (both an increase and a decrease can be observed), but the linear velocity of blood flow increases.

Systemic blood pressure in the first days of stay at heights increases slightly. The rise in systolic blood pressure is mainly caused by an increase in the IOC, and diastolic - by an increase in peripheral vascular resistance.

BCC increases due to the mobilization of blood from the depot.

Excitation of the sympathetic nervous system is realized not only by tachycardia, but also by paradoxical dilatation of the veins of the systemic circulation, which leads to a decrease in venous pressure at altitudes of 3200 and 3600 m.

There is a redistribution of regional blood flow.

The blood supply to the brain increases due to the reduction of blood flow in the vessels of the skin, skeletal muscles, and the digestive tract. The brain is one of the first to respond

for oxygen deficiency. This is due to the special sensitivity of the cerebral cortex to hypoxia due to the use of a significant amount of O 2 for metabolic needs (a brain weighing 1400 g consumes about 20% of the oxygen consumed by the body).

In the first days of alpine adaptation, the blood flow in the myocardium decreases.

The volume of blood in the lungs increases markedly. Primary high altitude arterial hypertension- an increase in blood pressure in the vessels of the lungs. The disease is based on an increase in the tone of small arteries and arterioles in response to hypoxia, usually pulmonary hypertension begins to develop at an altitude of 1600-2000 m above sea level, its value is directly proportional to the height and persists throughout the entire period of stay in the mountains.

An increase in pulmonary arterial blood pressure during ascent to a height occurs immediately, reaching its maximum in a day. On the 10th and 30th days, pulmonary BP gradually decreases, but does not reach the initial level.

The physiological role of pulmonary hypertension is to increase the volumetric perfusion of the pulmonary capillaries due to the inclusion of structural and functional reserves of the respiratory organs in gas exchange.

Inhalation of pure oxygen or a gas mixture enriched with oxygen at high altitude leads to a decrease in blood pressure in the pulmonary circulation.

Pulmonary hypertension, together with an increase in the IOC and the central blood volume, place increased demands on the right ventricle of the heart. At high altitudes, if adaptive reactions are disrupted, altitude sickness or acute pulmonary edema may develop.

Effect thresholds

The effect of oxygen deficiency, depending on the height and degree of extremeness of the terrain, can be divided into four zones (Fig. 6-3), delimited from each other by effective thresholds (Ruf S., Strughold H., 1957).

Neutral zone. Up to an altitude of 2000 m, the ability for physical and mental activity suffers little or does not change at all.

zone of full compensation. At altitudes between 2000 and 4000 m, even at rest, heart rate, cardiac output and MOD increase. The increase in these indicators while working at such heights occurs to a greater extent.

degree than at sea level, so that both physical and mental performance are significantly reduced.

Zone of incomplete compensation (danger zone). At altitudes from 4000 to 7000 m, an unadapted person develops various disorders. Upon reaching the violation threshold (safety limit) at an altitude of 4000 m, physical performance drops sharply, and the ability to react and make decisions weakens. Muscle twitching occurs, blood pressure decreases, consciousness gradually becomes clouded. These changes are reversible.

Rice. 6-3.Influence of oxygen insufficiency when ascending to a height: the numbers on the left are the partial pressure of O 2 in the alveolar air at the corresponding height; the figures on the right are the oxygen content in gas mixtures, which gives the same effect at sea level

Critical zone. Starting from 7000 m and above, in the alveolar air it becomes below the critical threshold - 30-35 mm Hg. (4.0-4.7 kPa). Potentially lethal disorders of the central nervous system occur, accompanied by unconsciousness and convulsions. These disturbances can be reversible provided rapid rise in inhaled air. In the critical zone, the duration of oxygen deficiency is of decisive importance. If hypoxia continues for too long,

violations occur in the regulatory links of the central nervous system and death occurs.

Long stay in the highlands

With a long stay of a person in high mountains at altitudes up to 5000 m, further adaptive changes in the cardiovascular system occur.

Heart rate, stroke volume and IOC stabilize and decrease to the initial values ​​and even lower.

Pronounced hypertrophy of the right parts of the heart develops.

The density of blood capillaries in all organs and tissues increases.

BCC remains increased by 25-45% due to an increase in plasma volume and erythrocyte mass. In high altitude conditions, erythropoiesis increases, so the concentration of hemoglobin and the number of red blood cells increase.

Natural adaptation of highlanders

The dynamics of the main hemodynamic parameters in the natives of the highlands (highlanders) at an altitude of up to 5000 m remains the same as in the inhabitants of the lowlands at sea level. The main difference between "natural" and "acquired" adaptation to high altitude hypoxia lies in the degree of tissue vascularization, microcirculation activity and tissue respiration. For permanent residents of the highlands, these parameters are more pronounced. Despite the reduced regional blood flow in the brain and heart in the natives of the highlands, the minute oxygen consumption by these organs remains the same as in the inhabitants of the plains at sea level.

CIRCULATION WITH EXCESS OF OXYGEN

Prolonged exposure to hyperoxia leads to the development of toxic effects of oxygen and a decrease in the reliability of adaptive reactions of the cardiovascular system. An excess of oxygen in the tissues also leads to an increase in lipid peroxidation (LPO) and the depletion of endogenous antioxidant reserves (in particular, fat-soluble vitamins) and the antioxidant enzyme system. In this regard, the processes of catabolism and deenergization of cells are enhanced.

The heart rate decreases, the development of arrhythmias is possible.

With short-term hyperoxia (1-3 kg X sec/cm -2) electrocardiographic characteristics do not go beyond the physiological norm, but with many hours of exposure to hyperoxia, the P wave disappears in some subjects, which indicates the appearance of an atrioventricular rhythm.

Blood flow in the brain, heart, liver and other organs and tissues is reduced by 12-20%. In the lungs, blood flow can decrease, increase, and return to its original level.

Systemic blood pressure changes slightly. The diastolic pressure usually rises. Cardiac output significantly decreases, and total peripheral resistance increases. The rate of blood flow and BCC during breathing with a hyperoxic mixture is significantly reduced.

The pressure in the right ventricle of the heart and pulmonary artery with hyperoxia often decreases.

Bradycardia in hyperoxia is mainly due to increased vagal influences on the heart, as well as the direct action of oxygen on the myocardium.

The density of functioning capillaries in tissues decreases.

Vasoconstriction during hyperoxia is determined either by the direct action of oxygen on vascular smooth muscles, or indirectly through a change in the concentration of vasoactive substances.

Thus, if the human body responds to acute and chronic hypoxia with complex and sufficiently effective complex adaptive reactions that form the mechanisms of long-term adaptation, then the effect of acute and chronic hyperoxia effective means the body has no protection.

CIRCULATION AT LOW EXTERNAL TEMPERATURES

There are at least four external factors that have a serious impact on human blood circulation in the conditions of the Far North:

Sharp seasonal, inter- and intra-day changes in atmospheric pressure;

Cold exposure;

A sharp change in photoperiodicity (polar day and polar night);

Fluctuations in the Earth's magnetic field.

The complex of climatic and ecological factors of high latitudes imposes stringent requirements on the cardiovascular system. Adaptation to conditions of high latitudes is divided into three stages:

Adaptive voltage (up to 3-6 months);

Stabilization of functions (up to 3 years);

Adaptability (up to 3-15 years).

Primary northern arterial pulmonary hypertension - the most characteristic adaptive reaction. An increase in blood pressure in the pulmonary circulation occurs at sea level under conditions of normal barometric pressure and O 2 content in the air. At the heart of such hypertension is the increased resistance of small arteries and arterioles of the lungs. Northern pulmonary hypertension is ubiquitous among visitors and indigenous populations of the polar regions and occurs in adaptive and maladaptive forms.

The adaptive form is asymptomatic, equalizes the ventilation-perfusion relationship and optimizes the oxygen regime of the body. Systolic pressure in the pulmonary artery with hypertension rises to 40 mm Hg, the total pulmonary resistance increases slightly.

maladaptive form. Latent respiratory failure develops - "polar shortness of breath", working capacity decreases. Systolic pressure in the pulmonary artery reaches 65 mm Hg, and the total pulmonary resistance exceeds 200 dynes Hsek X cm -5 . At the same time, the trunk of the pulmonary artery expands, pronounced hypertrophy of the right ventricle of the heart develops, while the stroke and minute volumes of the heart decrease.

CIRCULATION UNDER EXPOSURE TO HIGH TEMPERATURES

Distinguish adaptation in arid and humid zones.

Human adaptation in arid zones

Arid zones are characterized by high temperatures and low relative humidity. The temperature conditions in these zones during the hot season and in the daytime are such that the influx of heat into the body through insolation and contact with hot air can exceed heat generation in the body at rest by 10 times. Similar heat stress in the absence

effective mechanisms of heat transfer quickly leads to overheating of the body.

The thermal states of the body under conditions of high external temperatures are classified as normothermia, compensated hyperthermia and uncompensated hyperthermia.

hyperthermia- a borderline state of the body, from which a transition to normothermia or death (thermal death) is possible. The critical body temperature at which thermal death occurs in humans corresponds to + 42-43? C.

Action high temperature air per person, not adapted to the heat, causes the following changes.

Expansion of peripheral vessels is the main reaction to heat in arid zones. Vasodilation, in turn, should be accompanied by an increase in BCC; if this does not happen, then a drop in systemic blood pressure occurs.

The volume of circulating blood (VCC) at the first stages of thermal exposure increases. With hyperthermia (due to evaporative heat transfer), the BCC decreases, which entails a decrease in central venous pressure.

Total peripheral vascular resistance. Initially (the first phase), with a slight increase in body temperature, systolic and diastolic blood pressure decreases. The main reason for the decrease in diastolic pressure is a decrease in total peripheral vascular resistance. During heat stress, when the body temperature rises to +38 °C, the total peripheral vascular resistance decreases by 40-55%. This is due to dilatation of peripheral vessels, primarily of the skin. A further increase in body temperature (second phase), on the contrary, may be accompanied by an increase in total peripheral vascular resistance and diastolic pressure with a pronounced decrease in systolic pressure.

The heart rate (HR) increases, especially in poorly trained and poorly adapted people. In a person at rest at a high external temperature, the increase in the number of heartbeats can reach 50-80%. In well-adapted people, heat does not cause an increase in heart rate until heat stress becomes too severe.

Central venous pressure increases with an increase in body temperature, but thermal exposure can also cause the opposite effect - a transient decrease in the central blood volume and a persistent decrease in pressure in the right atrium. The variability of indicators of central venous pressure is due to the difference in the activity of the heart and BCC.

Minute volume of blood circulation (MOV) increases. The stroke volume of the heart remains normal or slightly decreases, which is more common. The work of the right and left ventricles of the heart when exposed to high external temperatures (especially with hyperthermia) increases significantly.

A high external temperature, which practically excludes all heat transfer pathways in a person, except for the evaporation of sweat, requires a significant increase in skin blood flow. The growth of blood flow in the skin is provided mainly by an increase in the IOC and, to a lesser extent, by its regional redistribution: under heat load at rest, the blood flow in the celiac region, kidneys, and skeletal muscles decreases in a person, which “frees” up to 1 liter of blood/min; the rest of the increased cutaneous blood flow (up to 6-7 liters of blood / min) is provided by cardiac output.

Intense sweating ultimately leads to dehydration of the body, thickening of the blood and a decrease in BCC. This puts additional stress on the heart.

Adaptation of migrants in arid zones. In the newly arrived migrants in the arid zones of Central Asia, when performing heavy physical work, hyperthermia occurs 3-4 times more often than among the natives. By the end of the first month of stay in these conditions, the indicators of heat exchange and hemodynamics in migrants improve and approach those of local residents. By the end of the summer season, there is a relative stabilization of the functions of the cardiovascular system. Starting from the second year, the hemodynamic parameters of the migrants almost do not differ from those of the local residents.

Aborigines of arid zones. Aborigines of arid zones have seasonal fluctuations in hemodynamic parameters, but to a lesser extent than migrants. The skin of the natives is richly vascularized, has developed venous plexuses, in which blood moves 5-20 times slower than in the main veins.

The mucous membrane of the upper respiratory tract is also richly vascularized.

Human adaptation in humid zones

Human adaptation in humid zones (tropics), where - except for elevated temperatures- high relative humidity, proceeds similarly to arid zones. The tropics are characterized by a significant tension in the water and electrolyte balance. For permanent residents of the humid tropics, the difference between the temperature of the "core" and "shell" of the body, hands and feet is greater than that of migrants from Europe, which contributes to a better removal of heat from the body. In addition, among the natives of the humid tropics, the mechanisms for generating heat with sweat are more perfect than among visitors. In aborigines, in response to a temperature exceeding +27 °C, sweating begins faster and more intensely than among migrants from other climatic and geographical regions. For example, in Australian aborigines, the amount of sweat evaporated from the surface of the body is twice that of Europeans in identical conditions.

CIRCULATION UNDER ALTERED GRAVITY

The gravitational factor has a constant effect on blood circulation, especially in the areas low pressure, forming the hydrostatic component of blood pressure. Due to the low pressure in the pulmonary circulation, the blood flow in the lungs largely depends on the hydrostatic pressure, i.e. gravitational effect of blood.

The model of the gravitational distribution of pulmonary blood flow is shown in fig. 6-4. In an upright adult, the tops of the lungs are located about 15 cm above the base of the pulmonary artery, so the hydrostatic pressure in the upper sections of the lungs is approximately equal to the arterial pressure. In this regard, the capillaries of these departments are slightly perfused or not perfused at all. In the lower parts of the lungs, on the contrary, hydrostatic pressure is combined with arterial pressure, which leads to additional stretching of the vessels and their plethora.

These features of the hemodynamics of the pulmonary circulation are accompanied by a significant unevenness of blood flow in different parts of the lungs. This unevenness significantly depends on the position of the body and is reflected in the indicators of regional saturation.

Rice. 6-4.A model that relates the uneven distribution of pulmonary blood flow in a vertical position of the human body with the pressure acting on the capillaries: in zone 1 (apex), the alveolar pressure (P A) exceeds the pressure in the arterioles (P a), and the blood flow is limited. In zone 2, where P a > P A , the blood flow is greater than in zone 1. In zone 3, the blood flow is increased and is determined by the pressure difference in arterioles (P a) and pressure in venules (Ru). In the center of the lung diagram are the pulmonary capillaries; vertical tubes on the sides of the lung - manometers

blood with oxygen. However, despite these features, in a healthy person, the saturation of the blood of the pulmonary veins with oxygen is 96-98%.

With the development of aviation, rocket technology and man's spacewalk, changes in systemic hemodynamics under conditions of gravitational overload and weightlessness become of great importance. Changes in hemodynamics are determined by the type of gravitational loads: longitudinal (positive and negative) and transverse.

QUESTIONS FOR SELF-CHECKING

1. What types of work can be distinguished by changes in heart rate?

2. What changes in the myocardium and regional circulation are observed during physical exertion?

3. By what mechanisms is the regulation of blood circulation carried out during physical exertion?

4. How does oxygen consumption change during exercise?

5. What changes occur in the circulatory system during hypokinesia?

6. Name the types of hypoxia depending on the duration of action.

7. What changes in the circulatory system are observed during adaptation to high mountains?

UDC 574.2:616.1

ENVIRONMENT AND CARDIOVASCULAR DISEASES

E. D. Bazdyrev and O. L. Barbarash

Research Institute of Complex Problems of Cardiovascular Diseases of the Siberian Branch of the Russian Academy of Medical Sciences, Kemerovo State medical Academy, Kemerovo

According to experts from the World Health Organization (WHO), the state of health of the population is determined by 49-53% by their lifestyle (smoking, drinking alcohol and drugs, diet, working conditions, physical inactivity, material and living conditions, marital status, etc.), by 18-22% - by genetic and biological factors, by 17-20% - by the state of the environment (natural and climatic factors, the quality of environmental objects) and only by 8-10% - by the level of healthcare development (timeliness and quality of medical care, efficiency preventive measures).

The high rates of urbanization observed in recent years with a decrease in the number of the rural population, a significant increase in mobile sources of pollution (motor transport), the mismatch of treatment facilities at many industrial enterprises with the requirements of sanitary and hygienic standards, etc. have clearly identified the problem of the impact of ecology on the state of public health.

Clean air is essential for human health and well-being. Air pollution continues to be a significant threat to human health around the world, despite the introduction of cleaner technologies in industry, energy and transport. Intensive air pollution is typical for large cities. The level of most polluting agents, and there are hundreds of them in the city, as a rule, exceeds the maximum permissible level, and their combined effect is even more significant.

Atmospheric air pollution is the cause of increased mortality of the population and, accordingly, a reduction in life expectancy. Thus, according to the WHO European Bureau, in Europe this risk factor led to a reduction in life expectancy by 8 months, and in the most polluted areas - by 13 months. In Russia, an increased level of atmospheric air pollution leads to an annual additional death rate of up to 40,000 people.

According to the Federal Information Center of the Fund for Social and Hygienic Monitoring, in Russia in the period from 2006 to 2010, the leading air pollutants exceeding hygiene standards by five or more times were: formaldehyde, 3,4-benz(a)pyrene, ethylbenzene, phenol, nitrogen dioxide, suspended solids, carbon monoxide, sulfur dioxide, lead and its inorganic compounds. Russia ranks 4th in the world in terms of carbon dioxide emissions after the US, China and EU countries.

Today, environmental pollution remains a significant problem throughout the world, is the cause of increased mortality and, in turn, a factor in the reduction of life expectancy. It is generally recognized that the influence of the environment, namely the pollution of the atmospheric basin with aeropollutants, causes mainly the development of diseases of the respiratory system. However, the impact on the body of various pollutants is not limited to changes in the bronchopulmonary system. In recent years, studies have appeared that prove the relationship between the level and type of air pollution and diseases of the digestive and endocrine systems. In the last decade, convincing data have been obtained on the adverse effects of air pollutants on the cardiovascular system. This review analyzes information both on the relationship of various diseases of the cardiovascular system with the impact of air pollutants, and on their possible pathogenetic relationships. Keywords: ecology, air pollutants, diseases of the cardiovascular system

In Russia, up to 50 million people live under the influence of harmful substances that exceed hygienic standards by five or more times. Despite the fact that since 2004 there has been a tendency to reduce the proportion of atmospheric air samples exceeding the hygienic standards of the average for Russian Federation, as before, this share remains high in the Siberian and Ural Federal Districts.

To date, it is generally recognized that the influence of the environment, namely the pollution of the atmospheric basin with aeropollutants, is the cause of the development of mainly diseases of the respiratory system, since most of all pollutants enter the body mainly through the respiratory organs. It has been proven that the effect of air pollutants on the respiratory organs is manifested by the suppression of the local defense system, the damaging effect on the respiratory epithelium with the formation of acute and chronic inflammation. It is known that ozone, sulfur dioxide, nitrogen oxides cause bronchoconstriction, bronchial hyperreactivity due to the release of neuropeptides from C-fibers and the development of neurogenic inflammation. It has been established that the average and maximum concentrations of nitrogen dioxide and the maximum concentrations of sulfur dioxide contribute to the development bronchial asthma.

However, the impact on the body of various pollutants is not limited to changes in the bronchopulmonary system. Thus, according to a study conducted in Ufa, as a result of an eight-year observation (2000-2008), it was shown that in the adult population there is a significant correlation between the level of atmospheric air pollution with formaldehyde and diseases endocrine system, the content of gasoline in the atmospheric air and general morbidity, including diseases of the digestive system.

In the last decade, convincing data have appeared on the adverse effects of air pollutants on the cardiovascular system (CVS). The first reports on the relationship of chemical pollutants with one of the significant risk factors for cardiovascular disease (CVD) - atherogenic dyslipidemia - were published back in the 80s of the last century. The reason for looking for associations was an even earlier study that showed an increase in mortality from coronary disease heart disease (CHD) almost 2 times in men with more than 10 years of experience exposed to carbon disulfide at work.

B. M. Stolbunov and co-authors found that in persons living near chemical enterprises, the incidence rate of the circulatory system was 2-4 times higher. A number of studies have examined the impact of chemical pollutants on the likelihood of not only

chronic, but acute forms ischemic heart disease. So, A. Sergeev et al. analyzed the incidence of myocardial infarction (MI) in people living near sources of organic pollutants, where the incidence of hospitalization was 20% higher than the frequency of hospitalizations of people not exposed to organic pollutants. In another study, it was found that the highest degree of “chemical contamination” of the body with toxic elements was noted in patients with MI who worked for more than 10 years in contact with industrial xenobiotics.

When conducting a five-year medical and environmental monitoring in the Khanty-Mansiysk Autonomous Okrug, a relationship was shown between the incidence of CVD and the level of air pollutants. Thus, the researchers drew a parallel between the frequency of hospitalizations for angina pectoris and an increase in the average monthly concentration of carbon monoxide and phenol. In addition, an increase in the level of phenol and formaldehyde in the atmosphere was associated with an increase in hospitalizations for MI and hypertension. Along with this, the minimum frequency of decompensation of chronic coronary insufficiency corresponded to a decrease in the concentration of nitrogen dioxide in the atmospheric air, the minimum average monthly concentrations of carbon monoxide and phenol.

Published in 2012, the results of studies conducted by A R. Hampel et al. and R. Devlin et al. showed an acute effect of ozone on the violation of myocardial repolarization according to ECG data. A study in London illustrated that an increase in the amount of pollutants in the atmosphere, especially with a sulfite component in patients with an implanted cardioverter-defibrillator, led to an increase in the number of ventricular extrasystoles, flutter and atrial fibrillation.

Undoubtedly, one of the most informative and objective criteria characterizing the state of health of the population is the mortality rate. Its value largely characterizes the sanitary and epidemiological well-being of the entire population. Thus, according to the American Heart Association, an increase in the level of dust particles with a size of less than 2.5 microns for several hours a week can be the cause of death in patients with CVD, as well as the cause of hospitalization for acute myocardial infarction and decompensation of heart failure. Similar data obtained in a study conducted in California, and in a twelve-year observation in China, showed that long-term exposure to dust particles, nitric oxide was not only a risk of developing coronary artery disease, stroke, but also a predictor of cardiovascular and cerebrovascular mortality.

A striking example of the relationship between CVD mortality and the level of air pollutants was the result of an analysis of the mortality structure of the population of Moscow during the anomalous summer of 2011. The increase in the concentration of pollutants in the atmosphere of the city had two peaks - on July 29 and August 7, 2011, reaching 160 mg/m3 and 800 mg/m3, respectively. At the same time, suspended particles with a diameter of more than 10 microns prevailed in the air. The concentration of particles with a diameter of 2.0-2.5 microns was especially high on June 29th. When comparing the dynamics of mortality with indicators of air pollution, there was a complete coincidence of the peaks in the number of deaths with an increase in the concentration of particles with a diameter of 10 microns.

Along with the negative impact of various pollutants, there are publications on their positive impact on the CCC. So, for example, the level of carbon monoxide in high concentrations has a cardiotoxic effect - by increasing the level of carboxyhemoglobin, but in small doses - cardioprotective against heart failure.

Due to the paucity of studies on the possible mechanisms of the negative impact of environmental pollution on CVS, it is difficult to draw a convincing conclusion. However, according to available publications, this interaction may be due to the development and progression of subclinical atherosclerosis, coagulopathy with a tendency to thrombosis, as well as oxidative stress and inflammation.

According to a number of experimental studies, the pathological relationship between lipophilic xenobiotics and IHD is realized through the initiation of lipid metabolism disorders with the development of persistent hypercholesterolemia and hypertriglyceridemia, which underlie arterial atherosclerosis. Thus, a study in Belgium showed that non-smoking patients with diabetes each doubling of distance from major highways was associated with a decrease in low-density lipoprotein levels.

According to other studies, xenobiotics themselves are capable of directly damaging the vascular wall with the development of a generalized immuno-inflammatory reaction that triggers the proliferation of smooth muscle cells, muscular-elastic intimal hyperplasia and fibrous plaque, mainly in small and medium-sized vessels. These vascular changes are called arteriosclerosis, emphasizing that the primary cause of the disorders is sclerosis, and not the accumulation of lipids.

In addition, a number of xenobiotics cause lability of vascular tone and initiate thrombus formation. A similar conclusion was reached by scientists from Denmark, who showed that the increase in the level of suspended particles in the atmosphere is associated with increased risk thrombosis.

As another pathogenetic mechanism underlying the development of CVD, the processes of free radical oxidation in areas of ecological trouble are being actively studied. The development of oxidative stress is a natural response of the body to the effects of xenobiotics, regardless of their nature. It has been proven that peroxidation products are responsible for initiating damage to the genome of vascular endothelial cells, which underlies the development of the cardiovascular continuum.

A study conducted in Los Angeles and Germany proved that long-term exposure to dust particles is associated with thickening of the intima/media complex as a sign of the development of subclinical atherosclerosis and an increase in blood pressure levels.

Currently, there are publications that testify to the relationship between genetic predisposition, inflammation, on the one hand, and cardiovascular risk, on the other. Thus, the high polymorphism of glutathione S-transferases, which accumulate under the influence of pollutants or smoking, increases the risk of a decrease in lung function over the course of life, the development of dyspnea and inflammation. Developed pulmonary oxidative stress and inflammation induce the development of systemic inflammation, which, in turn, increases cardiovascular risk.

Thus, it is possible that one of the possible pathogenetic links in the influence of environmental pollution on the formation of CVD is the activation of inflammation. This fact is also interesting in that in recent years, new data have appeared on the association of laboratory markers of inflammation with an unfavorable prognosis both in healthy individuals and in patients with CVD.

It is now generally accepted that the main cause of most types of respiratory pathology is inflammation. In recent years, data have been obtained indicating that an increase in the blood content of a number of non-specific markers of inflammation is associated with an increased risk of developing coronary artery disease, and with an already existing disease, with an unfavorable prognosis.

The fact of inflammation plays a major role in the development of atherosclerosis as one of the leading causes of coronary artery disease. It has been found that MI is more common among people with high level various inflammatory proteins in plasma, and decreased lung function is associated with increased level fibrinogen, C-reactive protein (CRP) and leukocytes.

Both in lung pathology (chronic obstructive pulmonary disease has been well studied in this regard), and in many CVDs (IHD, MI, atherosclerosis), there is an increase in the level of CRP,

interleukins-1p, 6, 8, as well as tumor necrosis factor alpha, and pro-inflammatory cytokines increase the expression of metalloproteinases.

Thus, according to the presented analysis of publications on the problem of the influence of environmental pollution on the occurrence and development of cardiovascular pathology, their relationship has been confirmed, but its mechanisms have not been fully studied, which should be the subject of further research.

Bibliography

1. Artamonova G. V., Shapovalova E. B., Maksimov S. A., Skripchenko A. E., Ogarkov M. Yu. Environment as a risk factor for the development of coronary heart disease in an urbanized region with a developed chemical industry // Cardiology. . 2012. No. 10. S. 86-90.

2. Askarova Z. F., Askarov R. A., Chuenkova G. A., Baikina I. M. Evaluation of the influence of polluted atmospheric air on the incidence of the population in an industrial city with developed petrochemistry // Zdravookhranenie Rossiiskoi Federatsii. 2012. No. 3. S. 44-47.

3. Boev V. M., Krasikov S. I., Leizerman V. G., Bugrova O. V., Sharapova N. V., Svistunova N. V. Influence of oxidative stress on the prevalence of hypercholesterolemia in an industrial city // Hygiene and sanitation. 2007. No. 1. S. 21-25.

4. Zayratyants O. V., Chernyaev A. L., Polyanko N. I., Osadchaya V. V., Trusov A. E. The structure of mortality of the population of Moscow from diseases of the circulatory and respiratory organs during the abnormal summer of 2010 // Pulmonology . 2011. No. 4. S. 29-33.

5. Zemlyanskaya O. A., Panchenko E. P., Samko A. N., Dobrovolsky A. B., Levitsky I. V., Masenko V. P., Titaeva E. V. Matrix metalloproteinases, C- reactive protein and markers of thrombopenia in patients with stable angina and restenoses after percutaneous coronary interventions. Cardiology. 2004. No. 11. S. 4-12.

6. Zerbino D. D., Solomenchuk T. N. Is atherosclerosis a specific arterial pathology or a “unified” group definition? Search for the causes of arteriosclerosis: an ecological concept // Archives of Pathology. 2006. V. 68, No. 4. S. 49-53.

7. Zerbino D. D., Solomenchuk T. N. The content of a number of chemical elements in the hair of patients with myocardial infarction and healthy people // Occupational Medicine and Industrial Ecology. 2007. No. 2. S. 17-21.

8. Karpin V. A. Medico-ecological monitoring of diseases of the cardiovascular system in the urbanized North // Cardiology. 2003. No. 1. S. 51-54.

9. Koroleva O. S., Zateyshchikov D. A. Biomarkers in cardiology: registration of intravascular inflammation // Farmateka. 2007. No. 8/9. pp. 30-36.

10. Kudrin A. V., Gromova O. A. Trace elements in neurology. M. : GEOTAR-Media, 2006. 304 p.

11. Nekrasov A. A. Immunoinflammatory mechanisms in heart remodeling in patients with chronic obstructive pulmonary disease. Journal of Heart Failure. 2011. V. 12, No. 1. S. 42-46.

12. Onishchenko GG On the sanitary and epidemiological state of the environment // Hygiene and Sanitation. 2013. No. 2. S. 4-10.

13. Assessment of the influence of environmental factors on the health of the population of the Kemerovo region: information and analytical review. Kemerovo: Kuzbassvuzizdat, 2011. 215 p.

14. Pulmonology [Kit]: national guideline with application on CD / ed. A. G. Chu-Chalina. M. : GEOTAR-Media, 2009. 957 p.

15. Revich B. A., Maleev V. V. Change of climate and health of the Russian population: Analysis of the situation. M. : LENAD, 201 1. 208 p.

16. Tedder Yu. R., Gudkov A. B. From environmental hygiene to medical ecology // Human Ecology. 2002. No. 4. S. 15-17.

17. Unguryanu T. N., Lazareva N. K., Gudkov A. B., Buzinov R. V. Evaluation of the medical and environmental situation in the industrial cities of the Arkhangelsk region // Human Ecology. 2006. No. 2. S. 7-10.

18. Unguryanu T. N., Novikov S. M., Buzinov R. V., Gudkov A. B. Public health risk from chemicals polluting the atmospheric air in a city with a developed pulp and paper industry // Hygiene and Sanitation. . 2010. No. 4. S. 21-24.

19. Khripach L. V., Revazova Yu. A., Rakhmanin Yu. A. The role of free radical oxidation in genome damage by environmental factors // Bulletin of the Russian Academy of Medical Sciences. 2004. No. 3. S. 16-18.

20. Shoikhet Ya. N., Korenovsky Yu. V., Motin A. V., Lepilov N. V. The role of matrix metalloproteinases in inflammatory diseases lungs // Problems of clinical medicine. 2008. No. 3. S. 99-102.

21. Anderson H. R., Armstrong B., Hajat S., Harrison R., Monk V., Poloniecki J., Timmis A., Wilkinson P. Air pollution and activation of implantable cardioverter defibrillators in London // Epidemiology. 2010 Vol. 21. R. 405-413.

22. Baker E. L. Jr., Landrigan P. J., Glueck C. J., Zack M. M. Jr., Liddle J. A., Burse V. W., Housworth W. J., Needham L. L. Metabolic consequences of exposure to polychlorinated biphenyls (PCB) in sewage sludge // Am. J. epidemiol. 1980 Vol. 112. R. 553-563.

23. Bauer M., Moebus S., Mohlenkamp S., Dragano N., Nonnemacher M., Fuchsluger M., Kessler C., Jakobs H., Memmesheimer M., Erbel R., Jockel K. H., Hoffmann B. Urban particulate matter air pollution is associated with subclinical atherosclerosis: results from the HNR (Heinz Nixdorf Recall) study // J. Am. Coll. cardiol. 2010 Vol. 56. R. 1803-1808.

24. Brook R. D., Rajagopalan S., Pope C. A. 3rd., Brook J. R., Bhatnagar A., ​​Diez-Roux A. V., Holguin F., Hong Y., Luepker R. V., Mittleman M. A., Peters A., Siscovick D., Smith S. C. Jr., Whitsel L., Kaufman J. D. American Heart Association Council on Epidemiology and Prevention. Council on the Kidney in Cardiovascular Diseases, end Council on Nutrition. Physical Activity and Metabolism. Particulate matter air pollution and cardiovascular disease: an update to the scientific statement from the American Heart Association // Circulation. 2010 Vol. 121. R. 2331-2378.

25. Devlin R. B., Duncan K. E., Jardim M., Schmitt M. T., Rappold A. G., Diaz-Sanchez D. Controlled exposure of healthy young volunteers to ozone causes cardiovascular effects // Circulation. 2012. Vol. 126. R. 104-111.

26. Engstrom G., Lind P., Hedblad B., Wollmer P., Stavenow L., Janzon L., Lindgarde F. Lung function and cardiovascular risk: relationship with inflammation-sensitive plasma proteins // Circulation. 2002 Vol. 106. R. 2555-2660.

27. Engstrom G., Lind P., Hedblad B., Stavenow L., Janzon L., Lindgarde F. Effects of cholesterol and inflammation-sensitive plasma proteins on incidence of myocardial infarction and stroke in men // Circulation. 2002 Vol. 105. P. 2632-2637.

28. Lind P. M, Orberg J, Edlund U. B, Sjoblom L., Lind L. The dioxin-like pollutant PCB 126 (3.3",4.4",5-p

entachlorobiphenyl) affects risk factors for cardiovascular disease in female rats // Toxicol. Lett. 2004 Vol. 150. P. 293-299.

29. Franchini M., Mannucci P. M. Thrombogenicity and cardiovascular effects of ambient air pollution // Blood. 2011 Vol. 118. P. 2405-2412.

30. Fuks K., Moebus S., Hertel S., Viehmann A., Nonnemacher M., Dragano N., Mohlenkamp S., Jakobs H., Kessler C, ErbelR., Hoffmann B. Long-term urban particulate air pollution , traffic noise, and arterial blood pressure // Environ. Health Perspective. 2011 Vol. 119. P. 1706-1711.

31. GoldD. R., Metteman M. A. New insights into pollution and the cardiovascular system 2010 to 2012 // Circulation. 2013. Vol. 127. P. 1903-1913.

32. HampelR., Breitner S., Zareba W., Kraus U., Pitz M., Geruschkat U., Belcredi P., Peters A., Schneider A. Immediate ozone affects on heart rate and repolarization parameters in potentially susceptible individuals / /Occup. Environ. Med. 2012. Vol. 69. P. 428-436.

33. Hennig B., Meerarani P., Slim R., Toborek M., Daugherty A., Silverstone A. E., Robertson L. W. Proinflammatory properties of coplanar PCBs: in vitro and in vivo evidence // Toxicol. Appl. Pharmacol. 2002 Vol. 181. P. 174-183.

34. Jacobs L., Emmerechts J., Hoylaerts M. F., Mathieu C., Hoet P. H., Nemery B., Nawrot T. S. Traffic air pollution and oxidized LDL // PLoS ONE. 2011. No. 6. P. 16200.

35. Kunzli N., Perez L., von Klot S., Baldassarre D., Bauer M., Basagana X., Breton C., Dratva J., Elosua R., de Faire U., Fuks K., de Groot E., Marrugat J., Penell J., Seissler J., Peters A., Hoffmann B. Investigation air pollution and atherosclerosis in humans: concepts and outlook // Prog. Cardiovasc. Dis. 2011 Vol. 53. P. 334-343.

36. Lehnert B. E., Iyer R. Exposure to low-level chemicals and ionizing radiation: reactive oxygen species and cellular pathways // Human and Experimental Toxicology. 2002 Vol. 21. P. 65-69.

37. Lipsett M. J., Ostro B. D., Reynolds P., Goldberg D., Hertz A., Jerrett M., Smith D. F., Garcia C., Chang E. T., Bernstein L. Long-term exposure to air pollution and cardiorespiratory disease in the California Teachers Study cohort // Am. J. Respir. Care Med. 2011 Vol. 184. P. 828-835.

38. Matsusue K., Ishii Y., Ariyoshi N., Oguri K. A. highly toxic PCB produces unusual changes in the fatty acid composition of rat liver // Toxicol. Lett. 1997 Vol. 91. P. 99-104.

39. Mendall M. A., Strachan D. P., Butland B. K, Ballam L., Morris J., Sweetnam P. M., Elwood P. C. C-reactive protein: relation to total mortality, cardiovascular mortality and cardiovascular risk factors in men // Eur. Heart J. 2000. Vol. 21. P. 1584-1590.

40. Schiller C. M, Adcock C. M, Moore R. A., Walden R. Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and fasting on body weight and lipid parameters in rats // Toxicol. Appl. Pharmacol. 1985 Vol. 81. P. 356-361.

41. Sergeev A. V., Carpenter D. O. Hospitalization rates for coronary heart disease in relation to residence near contaminated areas with persistent organic pollutants and other pollutants // Environ. Health Perspective. 2005 Vol. 113. P. 756-761.

42. Taylor A. E. Cardiovascular Effects of Environmental Chemicals Otolaryngology - Head and Neck // Surgery. 1996 Vol. 114. P. 209-211.

43. Tiller J. R., Schilling R. S. F., Morris J. N. Occupational

Toxic Factor in Mortality from Coronary Heart Disease // Br. Med. J. 1968. No. 4. P. 407-41 1.

44. Zhang P., Dong G., Sun B., Zhang L., Chen X., Ma N, Yu F, Guo H, Huang H, Lee Y. L, Tang N, Chen J. Long-term exposure to ambient air pollution and mortality due to cardiorespiratory disease and cerebrovascular disease in Shenyang China // PLoS ONE. 2011. No. 6. P. 20827.

1. Artamonova G. V., Shapovalova Je. B., Maksimov S. A., Skripchenko A. E., Ogarkov M. Ju. The Environment as a Risk Factor of Coronary Heart Disease in Urbanized Region With Developed Chemical Industry. Cardiology. 2012, 10, pp. 86-90.

2. Askarova Z. F., Askarov R. A., Chuenkova G. A., Bajkina I. M. Evaluation of the influence of polluted ambient air on morbidity in an industrial town with developed petrochemical industry. Zdravoohranenije Rossiiskoy Federatsii. 2012, 3, pp. 44-47.

3. Boev V. M., Krasikov S. I., Lejzerman V. G., Bugrova O. V., Sharapova N. V., Svistunova N. V. Impact of oxidative stress on the prevalence of hypercholesterolemia under the conditions of an industrial town. Gigiena i sanitarija. 2007, 1, pp. 21-25.

4. Zajrat "janc O. V., Chernjaev A. L., Poljanko N. I., Osadchaja V. V., Trusov A. E. Structure of mortality from cardiovascular and respiratory diseases during abnormal weather in summer, 2010, in Moscow. Pul "monologija . 2011, 4, pp. 29-33.

5. Zemljanskaja O. A., Panchenko E. P., Samko A. N., Dobrovol "skij A. B., Levickij I. V., Masenko V. P., Titaeva E. V. Matrix Metalloproteinases, C-Reactive Protein, and Markers of Thrombinemia in Patients With Stable Angina and Restenoses After Percutaneous Coronary Interventions. Kardiologija . 2004, 1 1, pp. 4-12.

6. Zerbino D. D., Solomenchuk T. N. Is atherosclerosis a specific arterial lesion or a "unified" group definition? Search for the causes of arteriosclerosis: an ecologic conception. Arhiv Patologii . 2006, 68 (4), pp. 4953.

7. Zerbino D. D., Solomenchuk T. N. Some chemical elements content of hair in post-infarction patients and healthy people. Meditsina truda ipromyshlennaya ekologija. 2007, 2, pp. 1721.

8. Karpin V. A. Medico-Ecological Monitoring of Cardiovascular Diseases in the Urbanized North. Cardiology. 2003, 1, pp. 51-54.

9. Koroleva O. S., Zatejshhikov D. A. Biomarkers in Cardiology: registration of intravascular inflammation. Farmateka. 2007, 8/9, pp. 30-36.

10. Kudrin A. V., Gromova O. A. Mikrojelementy v nevrologii. Moscow, GEOTAR-Media Publ., 2006, 304 p.

11. Nekrasov A. A. Immunoinflammatory mechanisms in heart remodeling in patients with chronic obstructive pulmonary disease. Zhurnal Serdechnaja nedostatochnost" . 2011, 12 (1), pp. 42-46.

12. Onishhenko G. G. On Sanitary and Epidemiological State of the Environment. Gigiena i sanitarija. 2013, 2, pp. 4-10.

13. Ocenka vlijanija faktorov sredy obitanija na zdorov "e naselenija Kemerovskoj oblasti: informacionno-analiticheskij obzor. Kemerovo, Kuzbassvuzizdat, 2011, 215 p.

14. Pul "monologija. Nacional" noe rukovodstvo s prilozheniem on kompakt-disk. Ed. A. G. Chuchalin. Moscow, GEOTAR-Media Publ., 2009, 957 p.

15. Revich B. A., Maleev V. V. Change klimata i zdorov "ja naselenija Rossii. Analiz situacii. Moscow, LENAD Publ., 201 1, 208 p.

16. Tedder J. R., Gudkov A. B. From the environment hygiene to medical ecology Ekologiya cheloveka . 2002, 4, pp.15-17.

17. Ungurjanu T. N., Lazareva N. K., Gudkov A. B., Buzinov R. V. Evaluation of medical-ecological situation tension in industrial cities of Arkhangelsk region. Ekologiya cheloveka. 2006, 2, pp.7-10.

18. Ungurjanu T. N., Novikov S. M., Buzinov R. V., Gudkov A. B. Human health risk of chemical air pollutants in a developed pulp and paper industry town. Gigiena i sanitarija. 2010, 4, pp. 21-24.

19. Hripach L. V., Revazova J. A., Rahmanin J. A. Active oxygen forms and genome damage by environmental factors. Vestnik RAMN. 2004, 3, pp. 16-18.

20. Shojhet Ja. N., Korenovskij J. V., Motin A. V., Lepilov N. V Role of matrix metalloproteinase in inflammatory diseases of the lungs. Problemy clinic meditsiny. 2008, 3, pp. 99-102.

21. Anderson H. R., Armstrong B., Hajat S., Harrison R., Monk V, Poloniecki J., Timmis A., Wilkinson P. Air pollution and activation of implantable cardioverter defibrillators in London. Epidemiology. 2010, 21, pp. 405-413.

22. Baker E. L. Jr., Landrigan P. J., Glueck C. J., Zack M. M. Jr., Liddle J. A., Burse V. W, Housworth W J., Needham L. L. Metabolic consequences of exposure to polychlorinated biphenyls (PCB) in sewage sludge. Am. J. epidemiol. 1980, 1 12, pp. 553-563.

23. Bauer M., Moebus S., Mohlenkamp S., Dragano N., Nonnemacher M., Fuchsluger M., Kessler C., Jakobs H., Memmesheimer M., Erbel R., Jockel K. H., Hoffmann B. Urban particulate matter air pollution is associated with subclinical atherosclerosis: results from the HNR (Heinz Nixdorf Recall) study. J. Am. Coll. cardiol. 2010, 56, pp. 1803-1808.

24. Brook R. D., Rajagopalan S., Pope C. A. 3rd., Brook J. R., Bhatnagar A., ​​Diez-Roux A. V., Holguin F., Hong Y., Luepker R. V., Mittleman M. A., Peters A., Siscovick D., Smith S. C. Jr., Whitsel L., Kaufman J. D. American Heart Association Council on Epidemiology and Prevention. Council on the Kidney in Cardiovascular Diseases, end Council on Nutrition. Physical Activity and Metabolism. Particulate matter air pollution and cardiovascular disease: an update to the scientific statement from the American Heart Association. circulation. 2010, 121, pp. 2331-2378.

25. Devlin R. B., Duncan K. E., Jardim M., Schmitt M. T., Rappold A. G., Diaz-Sanchez D. Controlled exposure of healthy young volunteers to ozone causes cardiovascular effects. circulation. 2012, 126, pp. 104-111.

26. Engstrom G., Lind P., Hedblad B., Wollmer P., Stavenow L., Janzon L., Lindgarde F. Lung function and cardiovascular risk: relationship with inflammation-sensitive plasma proteins. circulation. 2002, 106, pp. 2555-2660.

27. Engstrom G., Lind P., Hedblad B., Stavenow L.,

Janzon L., Lindgarde F. Effects of cholesterol and inflammation-sensitive plasma proteins on the incidence of myocardial infarction and stroke in men. circulation. 2002, 105, pp. 2632-2637.

28. Lind P. M., Orberg J., Edlund U. B., Sjoblom L., Lind L. The dioxin-like pollutant PCB 126 (3,3",4,4",5-p entachlorobiphenyl) affects risk factors for cardiovascular disease in female rats. Toxicol. Lett. 2004, 150, pp. 293-299.

29. Franchini M., Mannucci P. M. Thrombogenicity and cardiovascular effects of ambient air pollution. Blood. 2011, 118, pp. 2405-2412.

30. Fuks K., Moebus S., Hertel S., Viehmann A., Nonnemacher M., Dragano N., Mohlenkamp S., Jakobs H., Kessler C., Erbel R., Hoffmann B. Long-term urban particulate air pollution, traffic noise, and arterial blood pressure. Environ. Health Perspective. 2011, 119, pp. 1706-1711.

31. Gold D. R., Metteman M. A. New insights into pollution and the cardiovascular system 2010 to 2012. Circulation. 2013, 127, pp. 1903-1913.

32. Hampel R., Breitner S., Zareba W., Kraus U., Pitz M., Geruschkat U., Belcredi P., Peters A., Schneider A. Immediate ozone affects on heart rate and repolarization parameters in potentially susceptible individuals . Occup. Environ. Med. 2012, 69, pp. 428-436.

33. Hennig B., Meerarani P., Slim R., Toborek M., Daugherty A., Silverstone A. E., Robertson L. W. Proinflammatory properties of coplanar PCBs: in vitro and in vivo evidence. Toxicol. Appl. Pharmacol. 2002, 181, pp. 174-183.

34. Jacobs L., Emmerechts J., Hoylaerts M. F., Mathieu C., Hoet P. H., Nemery B., Nawrot T. S. Traffic air pollution and oxidized LDL. PLOS ONE. 2011, 6, p. 16200.

35. Kunzli N., Perez L., von Klot S., Baldassarre D., Bauer M., Basagana X., Breton C., Dratva J., Elosua R., de Faire U., Fuks K., de Groot E., Marrugat J., Penell J., Seissler J., Peters A., Hoffmann B. Investigation air pollution and atherosclerosis in humans: concepts and outlook. Prog. Cardiovasc. Dis. 2011, 53, pp. 334-343.

36. Lehnert B. E., Iyer R. Exposure to low-level chemicals and ionizing radiation: reactive oxygen species and cellular pathways. Human and Experimental Toxicology. 2002, 21, pp. 65-69.

37. Lipsett M. J., Ostro B. D., Reynolds P., Goldberg D., Hertz A., Jerrett M., Smith D. F., Garcia C., Chang E. T., Bernstein L. Long-term exposure to air pollution and cardiorespiratory disease in the California Teachers Study cohort. Am. J. Respir. Care Med. 2011, 184, pp. 828-835.

38. Matsusue K., Ishii Y., Ariyoshi N., Oguri K. A. highly toxic PCB produces unusual changes in the fatty acid composition of rat liver. Toxicol. Lett. 1997, 91, pp. 99-104.

39. Mendall M. A., Strachan D. P., Butland B. K., Ballam L., Morris J., Sweetnam P. M., Elwood P. C. C-reactive protein: relation to total mortality, cardiovascular mortality and cardiovascular risk factors in men. Eur. Heart J. 2000, 21, pp. 1584-1590.

40. Schiller C. M., Adcock C. M., Moore R. A., Walden R. Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and fasting on body weight and lipid parameters in rats. Toxicol. Appl. Pharmacol. 1985, 81, pp. 356-361.

41. Sergeev A. V., Carpenter D. O. Hospitalization rates for coronary heart disease in relation to residence near contaminated areas with persistent organic pollutants and other pollutants. Environ. Health Perspective. 2005, 113, pp. 756-761.

42. Taylor A. E. Cardiovascular Effects of Environmental Chemicals Otolaryngology - Head and Neck. surgery. 1996, 114, pp. 209-211.

43. Tiller J. R., Schilling R. S. F., Morris J. N. Occupational Toxic Factor in Mortality from Coronary Heart Disease. Br. Med. J. 1968, 4, pp. 407-41 1.

44. Zhang P., Dong G., Sun B., Zhang L., Chen X., Ma N., Yu F., Guo H., Huang H., Lee Y. L., Tang N., Chen J. Long- term exposure to ambient air pollution and mortality due to cardiorespiratory disease and cerebrovascular disease in Shenyang China. PLOS ONE. 2011, 6, p. 20827.

ECOLOGY AND CARDIOVASCULAR DISEASES

E. D. Bazdyrev, O. L. Barbarash

Research Institute for Complex Issues of Cardiovascular Diseases Siberian Branch RAMS, Kemerovo Kemerovo State Medical Academy, Kemerovo, Russia

Currently around the world, environmental pollution remains a significant problem causing increased mortality rates and a factor of reduced life expectancy. Admittedly, influence of the environment that is pollution of the atmosphere with air pollutants, results in preferential development of the respiratory system diseases. However, effects of different pollutants on human bodies are not limited to bronchopulmonary only

changes. Recently, a number of studies were conducted and proved a relation between levels and types of atmospheric air pollution and diseases of the digestive and endocrine systems. Earnest data about harmful effects of air pollutants on the cardiovascular system was obtained in the recent decade. In the review, there has been analyzed information both about the relation between different cardiovascular diseases and the aeropollutants" effects and their possible pathogenetic interrelations.

Keywords: ecology, air pollutants, cardiovascular diseases

Bazdyrev Evgeniy Dmitrievich - Candidate of Medical Sciences, Senior Researcher at the Department of Multifocal Atherosclerosis of the Federal State Budgetary Institution "Research Institute for Complex Problems of Cardiovascular Diseases" of the Siberian Branch of the Russian Academy of Medical Sciences, Assistant of the Department of Faculty Therapy, Occupational Diseases and Endocrinology, Kemerovo State Medical Academy of the Ministry healthcare of the Russian Federation

Address: 650002, Kemerovo, Sosnovy Boulevard, 6 E-mail: [email protected]

"The structure and work of the heart" - Humoral regulation of the work of the heart The activity of the heart is regulated by chemicals. Veins are vessels that carry blood to the heart. The total length of human capillaries is about 100,000 km. Automatism of the heart. What is a heart? "The structure and work of the heart." Cardiac cycle - 0.8 s Atrial contraction - 0.1 s Ventricular contraction - 0.3 s Relaxation of the ventricles and atria - 0.4 s.

"Work of the heart" - 0.3. Atria - ventricles. Blood from the ventricles enters the pulmonary artery and aorta. Blood from the veins enters the atrium and partially drains into the ventricles. 4. The valves are closed, the semilunar ones are open. What is a heart? Structure and function of the heart. Label the parts of the heart with numbers.

"Cardiovascular system" - Provides blood flow through blood vessels. The human cardiovascular system. The mass of the heart is approximately 220-300 g. The duration of the recovery period (in seconds). According to my research, the recovery process of heart rate is the smallest in children involved in sports. The form is determined by age, gender, physique, health, and other factors.

"The structure of the heart" - Find the vessels that flow into the right and left halves of the heart. Heart muscle. Right ventricle. The structure of the heart of fish. Aristotle. Locate the flap valves in the pictures. What is the heart covered with? The structure of the heart of reptiles. The structure of the heart of amphibians. Pulmonary artery. Left ventricle. Define the right and left halves of the heart.

"Human Heart" - Educational questions: What is the structure of the heart? The heart was and remains an organ that indicates the whole state of a person. Didactic goals of the project: What happens to the heart during various physical activities? Completed by: Mamontova Larisa Alexandrovna. What's happened cardiac cycle? Methodological tasks: What are the phases of the heart?

"Cardiac system" - The effect of smoking: vasospasm, impaired blood supply to organs, gangrene of the legs, etc. The main diseases of the cardiovascular system. Stop smoking and alcohol abuse. Rational and balanced nutrition. Hypodynamia - insufficient physical activity. Hygiene of the cardiovascular system.

In total there are 7 presentations in the topic