Adaptation is a systemic, stage-by-stage process of adapting an organism to factors of unusual strength, duration or nature (stress factors).

G. Selye singled out the general and local forms of the adaptation process. The general process is characterized by the involvement of all or most of the organs and physiological systems of the body in response. The local adaptation process is observed in individual tissues or organs during their alteration.

If the current stress factor is characterized by high intensity or excessive duration, then the development of the adaptation process can be combined with disturbances in the body's vital functions, the onset of disease or death.

Causes of the adaptation syndrome: exogenous and endogenous. Exogenous - physical (fluctuations in atmospheric pressure, temperature, physical activity, gravitational overload), chemical (starvation, intoxication with chemical substances, lack or excess of fluid intake into the body), biological (infection of the body, intoxication with biologically active substances). Endogenous - insufficiency of the functions of tissues, organs and their physiological systems, deficiency or excess of endogenous biologically active substances.

Stages: emergency adaptation, increased resistance, exhaustion.

The development of urgent (emergency) adaptation is based on the following mechanisms:

Activation of the nervous and endocrine systems. Stimulate catabolic processes in cells, the function of organs and tissues.

Increase in the content of Ca, cytokines, peptides.

Changes in the physicochemical state of the cell membrane apparatus, enzyme activity

The biological meaning is to create the conditions necessary for the body to "hold out" until the stage of formation of its stable increased resistance to the action of an extreme factor.

The second stage of long-term adaptation. Formation of stability, increase in the power and reliability of the functions of organs. Elimination of signs of stress reactions.

Stress is a generalized non-specific response of the body to the impact of various factors of an unusual nature, strength or duration.

Stages of stress: stage of anxiety, increased resistance, exhaustion

Stress (usually non-specific) reaction may include specific manifestations. For example, the formation of hormones in new ratios characteristic of a certain effect, or the synthesis of hormones that are new in structure and functions (not normally present in the body).

The specificity of the response of both the endocrine and other physiological systems to a particular effect can be manifested by various expressions of nonspecificity: quantitative (intensity of manifestation), temporal (terms and speed of occurrence) and spatial.

In response to the action of various stressors, not only adaptive, but also maladaptive stress reactions.

Both urgent and long-term adaptation of the body to the action of stress stimuli begins with disturbances in the body's homeostasis. Adaptation includes both specific and non-specific components and mechanisms.

Types of stress: adaptive and pathogenic. Adaptive, if the activation of organs and their systems under the action of a stress agent prevents violations of homeostasis, a state of increased resistance of the organism may form. Pathogenic stress - excessively prolonged or frequent repeated exposure to a strong stress agent on the body, which is not able to prevent a violation of homeostasis, can lead to significant life disorders and the development of an extreme or terminal state.

General etiology and mechanisms of damage to the nervous system. Systemic pathological phenomena: pathological dominant, parabiosis, limiting inhibition, the concept of a pathological system.

General etiology: exogenous causes - physical, chemical, biological nature, can be psychogenic. Endogenous - violation of blood and cerebrospinal fluid circulation in the brain, imbalance of biologically active substances or their effects, hypoxia, excessive activation of LPO, endocrine diseases, violation of thermal and water-electrolyte homeostasis of the body.

The main links of pathogenesis are: damage to neurons, violation of interneuronal interactions, disorder of the integrative activity of the nervous system.

Pathological parabiosis is a state of persistent (long-term), stationary, non-fluctuating excitation localized at the place of its occurrence, leading to a violation of conduction in one or another nervous structure of the body and having a negative effect on it. biological significance. Pathological parabiosis is accompanied by a partial or complete loss of the ability of the nervous structure to restore impaired functions, has a negative biological significance for the body, reduces its adaptive and resistogenic capabilities, as well as performance and life expectancy. Not yet. Vvedensky showed that different functional states (excitation, inhibition, death) develop in a neuromuscular preparation under the action of various damaging factors. Unlike physiological, pathological parabiosis is characterized by adverse consequences: - disorders of the functions of nerve formations; - restoration of nerve functions is limited - it is partial or not at all; - sometimes dysfunction of the nerve ends with its death; - decrease in adaptability, resistance and homeostasis of both nervous and other structures of the body as a whole. At the same time, pathological parabiosis has the same phases as physiological parabiosis (equalizing, paradoxical, narcotic, inhibitory, and ultraparadoxical).

Pathological dominant - the dominant focus of persistent excitation in a certain section of the central nervous system, which weakens the activity of neighboring nerve centers by "attracting" impulses addressed to neighboring centers to itself. As a result, significant and even irreversible changes occur, the adaptive capabilities of the organism are limited, its resistance and homeostasis decrease, and the restoration of its disturbed functions is only possible partially, or completely impossible. The pathological dominant, just like the pathological reflex and pathological parabiosis, plays an important role not only in aggravating the severity, but also in increasing the duration of certain diseases, pathological conditions, processes, trace reactions, as well as in their renewal (relapse). The pathological dominant is usually realized at the intercellular level. It usually leads to insufficiency of conjugate inhibition, and hence to the development of disorders of physiological systems, a decrease in certain functions of the central nervous system. The pathological dominant disrupts the integrative and adaptive activity of the nervous system. There are several types of pathological dominant: motor (motor), sensory (pain), food, sexual. The manifestation of the motor pathological dominant is muscle trembling (increased by inhalation and an increase in voluntary movements). Causalgia (burning pain) that occurs when a peripheral nerve is damaged and leads to the development of a focus of congestive excitation in various parts of the central nervous system (manifested, for example, in the form of pain in the limb in the zone of innervation of the damaged nerve) can serve as a manifestation of a painful pathological dominant.

A pathological system is a functional set of reactions of individual cells, tissues, organs, systems or the body as a whole, resulting from the impact on the body of a pathogenic factor, characterized by long-term self-sustaining activity and depression of sanogenetic mechanisms, which is based on a violation of the information process and leading (in the case of prolonged existence and progression) to deepening the imbalance of the diseased organism with the environment.

The pathological system is a new, that is, pathological integration that does not exist under physiological conditions, arising from primary and secondary altered formations of the central nervous system, the activity of which upsets the body's adaptation or causes pathological conditions and diseases. The formations and activity of the system are both the result and the mechanism for the further development of the pathological process. The pathological system determines the neuropathological syndrome.

Directly causes the formation of a pathological system hyperactive formation of the central nervous system, which acts as a pathological determinant. To the formation of a pathological system predispose:

1. Weakening of inhibitory control and an increase in the excitability of CNS formations, which are involved in the formation of a pathological system through the influence of a determinant.

2. Lack of systemic integrating regulatory influences in the CNS.

The role of the system-forming element of the pathological system of nervous regulation is played by the pathological determinant and its mechanism of hyperactivation in the form of a generator of pathologically enhanced excitation. Since the pathological set of neurons that form the pathological system is characterized by the insufficiency of inhibitory mechanisms, the activity of the pathological system is not regulated in accordance with the principle of negative feedback. Due to the hyperactivation of the backbone constellation of neurons of the pathological system and the secondary insufficiency of inhibitory mechanisms in their population, the pathological system is resistant to therapeutic effects.

The pathological system is capable of fixing through plastic processes and, as a rule, does not disappear after the reverse development of the behavioral disorders, emotions, homeostasis disorders and insufficiency of the useful adaptive result of functional systems caused by it.

Transmarginal inhibition occurs under the action of stimuli (stimuli) that excite the corresponding cortical structures above their inherent limit of working capacity, and thus provides a real possibility of its preservation or restoration.

In the scientific literature, the adaptation syndrome is characterized as a complex of changes that are unusual for a person, but manifest themselves when the body is exposed to various kinds of strong stimuli or factors that harm it.

ICD-10 code

F43 Severe stress response and adjustment disorders

Effects of glucocorticoids in general adaptation syndrome

Glucocorticoids are hormones that are released during the active work of the adrenal cortex. Their role is extremely important in the functioning of the body during the adaptation syndrome. They perform a protective function, which manifests itself in a decrease in the degree of vascular permeability, which prevents a decrease in blood pressure levels with negative stimuli. By reducing the permeability of cell membranes and lysosomes, glucocorticoids prevent their damage during injuries and poisoning. Also, thanks to them, the level of the body's energy resource increases, since these hormones are actively involved in the regulation of carbohydrate metabolism.

By reducing the degree of permeability of cells and blood vessels, glucocorticoids eliminate inflammatory processes. Another feature is that they increase the tone of the nervous system, supplying nerve cells with glucose. By activating the production of albumins in the liver, which are responsible for creating the desired level of blood pressure in the vessels, in stressful situations Glucocorticoids prevent a decrease in circulating blood volume and a drop in blood pressure.

But glucocorticoids are not always useful, they also have a damaging effect. They lead to the destruction of lymphoid tissue, which provokes the development of lymphopenia. This affects the production of antibodies. Therefore, it happens that physically healthy people begin to get sick more often.

In order not to face such an unpleasant condition as an adaptation syndrome, it is necessary to carry out stress prevention, namely to play sports, harden the body, attend auto-training, adjust the diet, pay attention to your favorite pastime. These methods will help to correct the body's response to mental stimuli, trauma, infection. The treatment process depends on the stage of the syndrome. At the first stage, hydroelectric solutions are used. On the second - potassium salts and hydrocortisone are prescribed. At the stage of exhaustion, restoration of the circulatory process will be required, therefore, cardiovascular analeptics are used.

Stress and adaptation syndrome

Adaptation syndrome is the body's response to stress. Experts have established factors that predispose to the development of this pathology:

• individual characteristics of a person: anxiety, low degree of stress resistance, nihilism, lack of initiative, social alienation,
• mechanisms of protection and resistance to stressful factors,
• social support or lack of it,
• An individual's prior prediction of an event that could have a stressful impact.

The reason for the appearance of an adaptation syndrome can be trauma, temperature changes, physical activity, infection, and so on. Among the main signs of the adaptation syndrome are: bleeding in the digestive organs, increased work and an increase in the size of the cortical layer of the adrenal glands, with an increased release of hormonal substances, involution of the thymus and spleen, and a decrease in the production of blood cells. It is possible to diagnose an adaptation disorder according to the following criteria:

• the appearance of a reaction to stress within 3 months from the moment of its manifestation;
• it is not a response to an unusual stressor, and goes beyond normal behavior;
• Violations in the professional and social spheres are obvious.

You can avoid the appearance of an adaptation syndrome in a natural way. Even experts prescribe medication as a last resort. It is necessary to develop a psychological defense mechanism, the main function of which is to develop conscious psychological barriers against negative emotions and factors that injure the psyche.

Selye's General Adaptation Syndrome

The famous physiologist, pathologist and endocrinologist Hans Selye put forward the theory that people exhibit non-specific physiological reactions of the body to stress. The combination of these reactions he gave the name - "general adaptation syndrome". The scientist determined that this manifestation is an enhanced adaptation of the body to changes in environmental conditions, due to the inclusion of special defense mechanisms.

Selye noted that no organism can be constantly in an alarming state. If stress has a strong effect, then the patient is expected to die even at the initial stage. At the second stage, adaptation reserves will be used up. If the stressor does not stop its action, then this leads to exhaustion. Selye argued that when the general adaptation syndrome is neglected, death can occur.

Stages of the adaptation syndrome

Three phases were distinguished in the adaptation syndrome:

• 1 - stage of anxiety. It can last from six hours to two days. At this time, the degree of production and entry into the bloodstream of glucocorticoids and adrenaline increases. The patient's body begins to adapt to the situation. The anxiety stage has two phases: shock and anti-shock. During the first, the degree of threat to the functional systems of the body increases, as a result of which hypoxia appears, blood pressure decreases, the temperature rises, and the level of glucose in the blood decreases. In the anti-shock phase, active work of the adrenal glands and the release of corticosteroids are observed.
• 2 - stage of resistance. The patient's resistance to various kinds of influences increases. Closer to its completion, the general condition of a person noticeably improves, the work of the systems returns to normal and recovery begins. If the strength of the stimulus significantly exceeds the capabilities of the organism, then it is impossible to talk about a positive result.
• 3 - stage of exhaustion. There is a high probability of death here, since the functional activity of the adrenal cortex weakens. Other systems are malfunctioning.

GENERAL ADAPTATION SYNDROME (STRESS)- nonspecific neurohumoral reaction of the body to the action of inadequate factors (stressors) of the external environment. The term "general adaptation syndrome" was proposed by the Canadian scientist G. Selye (1936), who gave an experimental justification for this concept.

O. a. With. or stress is usually called the reaction of activation of homeostatic mechanisms, and the processes that ensure the adaptation of the organism to activity in new conditions are called adaptation. The body responds to any extreme stimulus (high or low temperature, physical activity, pain, infection, hypoxia, etc.) complex reaction. It consists of a specific reaction, adequate to a given stimulus, and a general non-specific reaction, considered as a physiological (somatic) manifestation of O. a. With.

In response to a continuously acting stressor, three stages are distinguished: anxiety, resistance and exhaustion. They consistently reflect the mobilization of the body's defenses, adaptation to irritation and the decrease (exhaustion) of the body's reserve forces. In the general plan of O.'s development and. With. is determined by the biological and social significance of the stimulus, the reactivity of the organism and the reserves of its "adaptive energy".

Great importance is attached to the information content of the stressor, the subjective assessment of its signal value. There are two categories of stressors: some act directly on tissues, on the soma of the body and cause a state of physiological stress. Others act psychogenic, through the central receptors cause emotional and psychological reactions that cause emotional (psychophysiological) stress.

Of decisive importance are the states caused by negative emotions, overstrain of nervous mechanisms, caused by conflict situations. The signal for the involvement of the nervous mechanisms of negative emotions is the mismatch of the afferent model of the expected result with the afferentation about achieving the goal.

Not the quantitative and qualitative characteristics of the stressor in themselves, but its informative value, the psychological assessment of the signal as negative when a person is not prepared to avoid or protect, determine the occurrence of extreme emotional stress.

ADAPTATION SYNDROME

Accent placement: ADAPTATION SYNDROME

ADAPTATION SYNDROME (late Latin adaptatio - adaptation) - a set of non-specific changes that occur in the body of an animal or person under the influence of any pathogenic stimulus. Term proposed Selye(see) in 1936

According to Selye, A. s. is a clinical manifestation of the stress response (see Stress), which always occurs under any unfavorable conditions for the body.

Selye distinguishes between a general, or generalized, adaptation syndrome, the most severe manifestation of which is shock, and a local adaptation syndrome, which develops in the form of inflammation. The syndrome is called general (generalized) because it occurs as a reaction of the whole organism, and adaptive, since its development contributes to recovery.

In the development of general A. s. sequentially developing stages are noted. At first, when there is a threat of violation of homeostasis and the body's defenses are mobilized, the stage of anxiety occurs (anxiety is a call for mobilization). In the second phase of this stage, the disturbed balance is restored and the transition to the stage of resistance occurs, when the body becomes more resistant not only to the action of this stimulus, but also to other pathogenic factors (cross-resistance). In cases where the body does not completely overcome the ongoing action of a pathogenic stimulus, the stage of exhaustion develops. The death of the organism can occur in the stage of anxiety or exhaustion.

Rice. Changes in the body weight of growing rats at various stages of the general adaptation syndrome with dosed electrical stimulation: I - anxiety stage (mobilization phase); II - stage of resistance; III - stage of exhaustion

Change of the general balance of an exchange can serve as one of the indicators defining stages A. page. In the stage of anxiety and exhaustion, the phenomena of catabolism (dissimilation) predominate, and in the stage of resistance - anabolism (assimilation). In constantly growing animals (rats), the stages of general A. with., for example, with daily dosed electrical stimulation, can easily be detected by weight changes (Fig.). The most significant changes in the body with general AS: hypertrophy of the adrenal cortex, atrophy of the thymic-lymphatic system, and bleeding ulcers of the stomach and duodenum. These changes were known in the literature even before Selye's work. Hypertrophy of the adrenal cortex and an increase in its activity under the influence of various factors were studied by A. A. Bogomolets (1909). The appearance of hemorrhages in the stomach and intestines as a standard form of dystrophy was described by AD Speransky (1935). Selye sought to find the causes of the general A. s. and determine its biological nature. Part of this very difficult task was successfully solved by him. It has been established that many of the changes that occur with general A. of page depend on the increase in the hormonal activity of the anterior pituitary gland, which, releasing adrenocorticotropic hormone (ACTH), stimulates the secretory activity of the adrenal cortex. Many researchers have shown that the reaction of the anterior pituitary and adrenal cortex occurs very quickly (minutes and even seconds) and that, in turn, it depends on the hypothalamus, in which a special substance is produced - the releasing factor (see Fig. hypothalamic neurohormones), stimulating the secretion of the anterior pituitary gland. Thus, with general A. s. the system reacts hypothalamus → anterior pituitary → adrenal cortex. The release of adrenaline and norepinephrine should be attributed to the number of triggers of this system, the value of which, regardless of the work of Selye, was shown by Kennop (W. Cannon, 1932), as well as L. A. Orbeli (1926 - 1935) in the doctrine of adaptive -trophic role of the sympathetic nervous system.

It has been firmly established in experiments and in the clinic that with functional insufficiency of the adrenal cortex, the body's resistance sharply decreases. The introduction of steroid hormones (glucocorticoids) can restore the body's resistance, so Selye considers them adaptive hormones. He also includes ACTH, STH, epinephrine and norepinephrine in the same group, since their action is associated with the adrenal glands and adaptation. However, in the works of Selye it is shown that certain hormones and drugs (ethyl esternol, tyrosine, etc.) can increase the body's resistance to toxic substances, enhancing the action of liver enzyme systems. In this regard, it should not be assumed that the state of nonspecific resistance of the organism is determined only by the direct action of the hormones themselves on the pathogenic factor. The state of nonspecific resistance depends on a number of processes. This includes the effect of hormones on inflammation, vascular permeability, enzyme activity, the blood system, etc.

A lot of unclear and in the explanation of the mechanism of occurrence of various symptoms of general A. s. At first, it was believed that atrophy of the thymic-lymphatic system occurs as a result of the disintegration of lymphoid cells under the influence of an increase in glucocorticoids in the blood, which always takes place in the initial phase of the development of general A. s. However, it has been established that the breakdown of lymphoid cells is not so great and that the main factor in tissue devastation is the migration of lymphoid cells.

The formation of gastric and duodenal ulcers cannot be made directly dependent on the secretory activity of the adrenal cortex. The occurrence of ulcers is largely associated with the influence of the autonomic nervous system on the acidity and enzymatic activity of gastric juice, mucus secretion, muscle wall tone and changes in microcirculation. In order to clarify ulcerogenic mechanisms, the significance of mast cell degranulation, an increase in histamine(mass media serotonin(see) and influence of microflora. However, the question of which factor is decisive in the development of ulcers and what role corticosteroids play in these processes has not yet been resolved. It cannot be considered that the formation of ulcers is an adaptive process. Neither the mechanisms of development, nor the biological significance of this phenomenon in the concept of general A. s. not disclosed. However, the use of corticosteroids in large, non-physiological doses can cause the development of gastric and duodenal ulcers.

Selye rightly believes that the protective reactions of the body are not always optimal, therefore, in many cases, in his opinion, so-called. adaptation diseases. The main reason for their development, according to Selye, is either an incorrect ratio of hormones, with Krom hormones that enhance the inflammatory response prevail (STH of the pituitary gland and mineralocorticoids of the adrenal cortex), while anti-inflammatory hormones (ACTH of the pituitary gland and glucocorticoids of the adrenal cortex) are not enough, or special reactivity of the body caused by adverse previous effects (nephrectomy, excessive salt load, the use of corticosteroids, etc.), which creates a predisposition (diathesis) to the development of pathological processes. Under the experimental conditions, it was possible to reproduce a number of diseases such as collagenoses, arthritis, periarteritis nodosa, nephrosclerosis, hypertension, myocardial necrosis, scleroderma, muscle tissue metaplasia, etc. However, there is no reason to believe that the causes of certain processes in the experiment are identical to the causes of their appearance. in the human body.

So, in the clinic with these pathological processes, an increase in the number of pro-inflammatory corticoids (DOCA, aldosterone, growth hormone) was not found, which was to be expected according to Selye's concept. At many hron. human diseases, there are no changes characteristic of adaptation diseases. The critical analysis of nek-ry experiments of Selye suggests that sometimes the arising pathology is a consequence rather of allergic manifestations, than hormonal disorders [Cope (C. L. Sore)]. And if inadequate hormonal reactions take place, then they should rather be considered as a manifestation of the pathology of the corresponding glands than as an adaptation disease.

In works on the study of local adaptation syndrome, Selye showed that, depending on changes in the hormonal activity of the pituitary gland and adrenal cortex, the barrier role of inflammation can change significantly.

Selye considers the general A. s. an obligatory manifestation of "just a disease." Therefore the same picture of the general And. is a common component in a variety of diseases, not related to the specifics of the action of the pathogenic factor. On this basis, Selye has been promoting the idea of ​​building a unified theory of medicine for many years, and this undoubtedly arouses great interest. However, not all of Selye's theoretical generalizations are universally accepted. In any nonspecific reaction, there are always characteristic signs due to the action of this particular stimulus, so the reactions are not unambiguous, and the development of A. s. not due to a single mechanism of hormonal influences (eg, gastric and duodenal ulcers). similarity external manifestations general A. s. in various diseases does not serve as proof of the commonality of etiological causes, therefore Selye's idea of ​​pluricausalism as the basis for the development of all diseases cannot be unconditionally accepted.

Bibliographer.: Horizons P. D. The role of the pituitary - adrenal cortex in the pathogenesis of extreme conditions, Vesti. USSR Academy of Medical Sciences, No. 7, p. 23, 1969, bibliogr.; Horizons P. D. and Protasova T. N. The role of ACTH and corticosteroids in pathology (To the problem of stress), M., 1968, bibliogr.; Selye G. Essays on the adaptation syndrome, trans. from English, M., I960; he is, At the level of the whole organism, trans. from English, M., 1972; Cope C. L. Adrenal steroids and disease, L., 1965, bibliogr.

1. Big medical encyclopedia. Volume 1 / Editor-in-Chief Academician B. V. Petrovsky; publishing house "Soviet Encyclopedia"; Moscow, 1974.- 576 p.

General adaptation syndrome

Psychology. AND I. Dictionary-reference book / Per. from English. K. S. Tkachenko. - M.: FAIR-PRESS. Mike Cordwell. 2000 .

See what the "General Adaptation Syndrome" is in other dictionaries:

General adaptation syndrome- is the reaction of the individual to severe stress. See Adaptation Syndrome. * * * - G. Selye's term refers to the three-stage characteristic of the body's biological response to severe stress discovered and studied by him and his scientific school (as physical ... Encyclopedic Dictionary of Psychology and Pedagogy

GENERAL ADAPTATION SYNDROME- A term referring to the physiologist Hans Selye's theory of a three-step characterization of the body's biological responses to severe stress. The first stage, the alarm reaction, is characterized by two substages, the shock phase and the countercurrent phase. During ... ... Explanatory Dictionary of Psychology

General adaptation syndrome- Hans Selye suggested that all people exhibit the same non-specific physiology. response to stress. He called the totality of these reactions O. a. With. According to Selye, the general reactions of the body are similar, no matter what they call stress, although ... ... Psychological Encyclopedia

General adaptation syndrome OSA (honey) -- a set of adaptive reactions of the body to adverse effects (stressors) that are significant in strength and duration. This term was proposed in 1936 by G. Selye. There are three stages in the development of OSA: stage I of anxiety; Stage II ... ... Dictionary-reference book of philosophy for students of medical, pediatric and dental faculties

ADAPTATION SYNDROME- (general adaptation syndrome) a set of protective reactions of the human or animal body (mainly the endocrine system) under stress. In the adaptation syndrome, stages of anxiety (mobilization of protective forces), resistance are distinguished ... ... Big Encyclopedic Dictionary

ADAPTATION SYNDROME- General adaptation syndrome, a set of changes that occur in the body under stress. In humans and higher animals, three phases of A. with are distinguished: anxiety, resistance, and exhaustion. For the anxiety phase of the body's primary response to action ... ... Biological Encyclopedic Dictionary

Adaptation Syndrome- general adaptation syndrome, a set of general protective reactions that occur in the body of animals and humans under the influence of external and internal stimuli that are significant in strength and duration; these reactions contribute to ... ... Great Soviet Encyclopedia

ADAPTATION SYNDROME- (general adaptation syndrome), a set of protective reactions of the human or animal body (primarily the endocrine system) under stress. You. distinguish between stages of anxiety (mobilization of protective forces), resistance (adaptation to difficult ... ... Natural science. Encyclopedic Dictionary

adaptation syndrome- (general adaptation syndrome), a set of protective reactions of the human or animal body (mainly the endocrine system) under stress. In the adaptation syndrome, there are stages of anxiety (mobilization of protective forces), resistance ... ... Encyclopedic Dictionary

ADAPTATION SYNDROME- See general adaptation syndrome ... Explanatory Dictionary of Psychology

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G Selye General Adaptation Syndrome

Chapter 3. GENERAL ADAPTATION SYNDROME

The idea of ​​stress (from the English stress - tension) as a general adaptation syndrome (GAS) was first formulated by the prominent Canadian scientist Hans Selye (1907-1982).

Stress is a special state of the body that occurs in response to the action of any stimuli that threaten homeostasis, and is characterized by the mobilization of non-specific adaptive reactions to ensure adaptation to the acting factor.

As a stressor, that is, an agent that causes stress, any external or internal stimuli can act, ordinary or unusual in nature, but placing increased demands on the body, actually violating or potentially threatening the constancy of the internal environment of the body. Any surprise that disrupts the usual course of life can be a cause of stress. These are psychosocial, industrial, everyday difficulties that must be overcome, infection, pain factors, heavy physical exertion, high temperature or cold, hunger, weakness, hypoxia, and even unpleasant memories. Here is how Selye himself wrote about the causes of stress: “Everything pleasant and unpleasant that speeds up the rhythm of life can lead to stress. A painful blow and a passionate kiss can equally cause it.

So, from the point of view of the stress reaction, it does not matter the nature of the demand made on the body, whether it is unexpected joy or conflict situation life-threatening or causing a negative emotional state - fear, mental discomfort, etc. For the formation of a stress reaction, the strength of the stress effect does not matter. Decisive for the occurrence of a stress reaction is only whether the stimulus makes additional demands on the body, whether it causes the need for adaptation, the inclusion of new adaptive mechanisms. However, the severity of the stress reaction will, of course, depend on the intensity, duration, and frequency of exposure to the stress factor. In addition, the intensity of the stress response will be determined by the adaptive potential of the organism itself, its adaptive capabilities.

The action of a stress stimulus induces the development of a general adaptation syndrome. OAS is a manifestation of stress in its temporal development, therefore, OSA should be understood as a set of non-specific adaptive reactions that occur in response to the action of a stress factor and are aimed at overcoming the adverse effect of this agent on health.

G. Selye identified three stages in the development of the OAS.

The first stage of OSA is the alarm reaction stage. This is the stage of formation of adaptation reactions. The alarm reaction means the immediate mobilization of the body's protective resources and the simultaneous suppression of those functions that are less important for the survival of the body under the influence of a stressor, in particular, growth, regeneration, digestion, reproductive functions, lactation. This stage is characterized by the tension of the functions of various structures due to the mobilization of available reserves. The body prepares to counter the stress factor and, if these reserves are sufficient, then adaptation develops rapidly.

What is the trigger of the stress response?

The influence of any stressor is transmitted directly through extero-, interoreceptors and afferent nerve pathways, or humorally to the central nervous structures that control the adaptive activity of the body. These structures are located in the cerebral cortex, in the reticular formation of the brain stem, in the limbic system. In these structures, the analysis of nervous and humoral influences caused by the action of a stressor is carried out, and their emotional coloring occurs. The response formed in the above structures is transmitted to various target organs, which ensure the development of changes specific to a given stressor in the body related to its quality, as well as non-specific shifts that are the body's response to the requirement presented to it as such, regardless of its nature. According to G. Selye, it is these non-specific changes that make up the essence of stress and manifest themselves in the form of a general adaptation syndrome.

The decisive role in the formation of OSA is played by the hypothalamus, the activation of which occurs under the action of any stressor. The hypothalamus is an organ of the central nervous system, which, having received information about the appearance of a stressor, starts the work of the entire stress system, coordinates the endocrine, metabolic and behavioral reactions of the body to stressors. Activation of the anterior and middle nuclei of the hypothalamus leads to the release of the so-called releasing factors, liberins, or, as they are now more commonly called, regulatory hormones that direct the function of the anterior pituitary gland, its secretion of tropic hormones. In particular, when CRH neurons of the paraventricular nucleus of the anterior hypothalamus are activated, corticotropin-releasing hormone is released, which stimulates the synthesis and secretion of adrenocorticotropic hormone (ACTH). The latter, in turn, stimulates an increased release of glucocorticoids (GC) from the fascicular zone of the adrenal cortex - cortisol (hydrocortisone) and corticosterone, the most active and significant for humans.

Activation of the posterior hypothalamus leads to an increase in the tone of the sympathetic-adrenal system. At the same time, the tone of the sympathetic nervous system increases, the release of norepinephrine from the sympathetic nerve endings increases, and adrenaline is released from the adrenal medulla into the blood, which leads to a significant increase in the level of catecholamines (CH) in the blood.

Thus, stress stimuli cause, first of all, activation of the hypothalamic-pituitary-adrenal system (HPAS), excessive production of adaptive hormones, from which the organization of protection against the action of a stress factor begins. These are substances such as HA, adrenaline, norepinephrine (G. Selye, 1960, 1979)

Other hormones and biologically active substances also take part in the formation of stress. G. Selye himself admitted that the HPA, although it plays a leading role in the development of stress, is nevertheless not the only system responsible for all manifestations of the stress reaction. Thus, it was found that the activation of the anterior hypothalamus under the influence of stress factors is accompanied by an increase in the production of arginine-vasopressin. Vasopressin is considered as a factor that potentiates the effect of corticoliberin and promotes the release of ACTH, as well as increasing the activity of the sympathetic nervous system, which enhances its effect during stress (Tigranyan R.A., 1988)

Activation of the hypothalamus and sympathetic nervous system also contributes to increased secretion of β-endorphins from the intermediate lobe of the pituitary gland and methenkephalins from the adrenal glands. (Tigranyan R.A., Vakulina O.P., 1984; Pshennikova M.G., 1987). According to modern concepts, opioid peptides are involved in the regulation of the activity of neurons in the CNS structures that form stress reactions, in particular, they regulate the secretion of hypothalamic hormones and adenohypophysis hormones, they are modulators of the activity of the adrenal cortex, and they inhibit the processes of release and reception of catecholamines.

The question of the activation of the production of thyroid-stimulating hormone (TSH) by the pituitary gland and functional activity thyroid gland under stressful influences remains controversial. According to most authors, the function of the thyroid gland is inhibited under stress, which is associated with the suppression of TSH secretion under the influence of high concentrations of ACTH (Laykok J.F., Weiss P.G., 2000). Others, on the contrary, found an increase in TSH secretion and an increase in thyroid function, especially in experiments with exposure to low temperatures(Horizontov P.D., 1981). The inconsistency of data on the role of the thyroid endocrine system in the development of stress is apparently explained by the fact that the nonspecific effects of a stressor under certain circumstances can be modified by its specific properties.

A certain role in the development of the stress response belongs to glucagon, the secretion of which increases under the influence of catecholamines. At the same time, an excess of CH inhibits the production of another pancreatic hormone - insulin. Under stress, an increase in the level of parathyroid hormone is naturally noted, due to which calcium is mobilized from the bones and its level in the blood and cells increases, where it is a universal stimulator of intracellular processes.

In recent years, it has been shown that a number of biologically active substances are involved in the stress reaction, potentiating or mediating the effects of the main realizing links of the stress system. These are substances such as angiotensin II, some interleukins, neuropeptide Y, substance P. The mechanisms of action of the above substances in adaptation reactions are still poorly understood.

The stage of anxiety occurs at the time of the action of the stressor, it can last for 48 hours after the onset of the stressor. Its severity depends on the strength and duration of the stimulus. The anxiety stage is divided into two phases: shock (shock) and countershock. In the shock phase, there is a threat to all vital functions of the body, while hypoxia, arterial hypotension, muscle hypotension, hypothermia, hypoglycemia develop, catabolic reactions in tissues predominate over anabolic ones. At this stage, the secretion of catecholamines, glucocorticoids increases, but on the other hand, the need for HA in tissues increases to an even greater extent, since the degree of their utilization by tissues sharply increases. The latter leads to a relative insufficiency of HA, despite their increased production. During this period, the body's resistance decreases, and if the actions of the stressor go beyond the compensatory capabilities of the body, then death may occur already at this stage. But if adaptation mechanisms prevail, then the countershock phase begins. This phase is due to a sharp hypertrophy of the fascicular zone of the adrenal cortex, increased secretion of HA and an increase in their level in the blood and tissues.

If the effect of the stressor is not very strong, then the countershock phase may develop immediately without a preliminary shock phase. The countershock phase is a transitional stage to the next stage of the OSA - the stage of resistance.

The resistance stage is characterized by a restructuring protective systems body adapting to the stressor. The body's resistance rises above the norm, and not only to the agent that caused stress, but also to other pathogenic stimuli. This indicates the non-specificity of the stress reaction. At this stage, new interendocrine relationships are established. Enhanced production of adaptive hormones - catecholamines, HA continues, although the level of their secretion decreases compared to the first stage. Catecholamines increase the secretion of glucagon and inhibit the production of insulin, resulting in a significant decrease in the level of insulin in the blood. The production of somatotropic hormone, prolactin, sharply increases (Zaichik A.Sh., Churilov A.P., 2001). By this moment, specific homeostatic reactions characteristic of this stress factor develop and are activated.

In the event of the termination of the influence of the stress agent or the weakening of its strength, the changes caused by them in the body (hormonal, structural and metabolic changes) gradually normalize. There are no pronounced pathological consequences.

When the pathogenic stimulus has excessive strength or acts for a long time, repeatedly, then the adaptive capabilities of the organism may turn out to be untenable. This will cause a loss of resistance and the development of the final stage of OSA - the stage of exhaustion (stage of exhaustion). First of all, we are talking about the depletion of the fascicular zone of the adrenal cortex, its progressive atrophy and a decrease in the production of HA. This stage is characterized by a decrease in the activity of the sympathetic-adrenal system, inhibition of all protective processes in the body, low resistance of the body to any stressors. At this stage, changes appear that are characteristic of the stage of anxiety, but if at the stage of anxiety these changes are reversible, then at the stage of exhaustion they are often irreversible and often lead the body to death. At this stage, an absolute insufficiency of HA develops, due to the depletion of the fascicular zone of the adrenal cortex. Minera-locorticoids predominate in this stage, which in many respects are GC antagonists. The stage of exhaustion characterizes the transition of an adaptive stress response to pathology.

How, then, do glucocorticoids increase the body's resistance, fulfilling their adaptive role under the influence of various stress factors?

The main mechanisms for urgent adaptation provided by the Civil Code are:

1. Mobilization and directed redistribution of energy resources of the body. HA, together with CH, provide rapid energy supply to tissues involved in adaptation to a given stressor. The level of energy consumption of the body under severe stress can exceed the basic metabolism by 2 times.

Energy reinforcement of adaptive reactions is carried out primarily due to the fact that HA and CH activate gluconeogenesis in the liver (6-10 times) - the formation of glucose from non-carbohydrate products - amino acids and fatty acids. Muscle proteins and fatty acids become the main endogenous sources of energy. Thus, the plastic, building material, which are proteins and fats, is converted into energy. HA and CK (especially epinephrine) also weaken the effect of insulin on glucose uptake by insulin-dependent organs and tissues, which contributes to hyperglycemia. CH, activating phosphorylase, accelerates the processes of glycogenolysis and the release of glucose, especially from the liver, into the systemic circulation. At the same time, GCs, unlike CCs, cause the accumulation of glycogen in the liver, thereby preventing the depletion of energy resources of liver cells.

Under the influence of HA and CH, the mobilization of fats from fat depots is enhanced, lipolysis is activated in adipose tissue, which leads to an increase in the level of non-esterified fatty acids in plasma. This allows some organs and tissues to start using them as an energy substrate. Under stress, β-oxidation of fatty acids in the myocardium, skeletal muscles, kidneys, and nervous tissue increases.

Thus, a significant amount of glucose, fatty acids, the main sources of energy, are released into the blood, which are so necessary at the moment to ensure the increased functions of the body to eliminate the effects of the stress factor.

2. Mobilization and directed redistribution of the body's protein reserve. In tissues that are not involved in adaptation, especially in lymphoid, muscle, connective and bone, there is inhibition of protein synthesis, partial cell lysis. In the liver, central nervous system and heart, protein synthesis is not limited. The amino acids released in catabolism reactions are directed mainly to the liver, where they are used in gluconeogenesis reactions, as well as for the synthesis of enzymatic proteins. Due to the regulation of activity and the synthesis of enzymatic proteins, HA are involved in a wide range of metabolic processes. In addition, part of the amino acids is used for the synthesis of structural proteins in the cells of organs and tissues responsible for adaptation to the action of a stressor. This leads to the formation of structural changes in them (for example, hypertrophy of the cardiac and skeletal muscles during exercise), which significantly increase the power of the reacting systems.

3. Selective distribution of circulating blood. Due to the narrowing of the vessels of organs that are not involved in adaptation (for example, abdominal organs and inactive muscles), blood is directed to the organs involved in adaptation.

4. Enrichment of blood with oxygen and an increase in the flow of oxygen to the tissues due to increased ventilation of the lungs and an increase in cardiac output.

5. Activation of intracellular processes by a moderate increase in the content of calcium in the cytoplasm of cells - a universal stimulator of cell function, as well as by activation of regulatory enzymes - protein kinases. This is due to an increase in the parathyroid hormone in the blood, under the influence of which calcium is released from the bone tissue and its increase in the blood, as well as the activation of the mechanisms of calcium entry into the cell, which is provided by an increased level of CH, HA, vasopressin.

6. Potentiation of the action of CH. HA enhance the effect of catecholamines and thereby increase the effectiveness of adaptive reactions mediated by them. Due to their potentiating (permissive) action, HAs are able to inhibit vascular disorders, have a tonic effect on blood vessels, help increase the total peripheral vascular resistance and systemic blood pressure, cardiac output, and prevent the development of acute vascular insufficiency.

7. Increasing the stability and power of the cell ion pumps. Under the influence of HA, the synthesis of enzymes that provide trans-membrane movement of ions increases, the activity of the main lipid-dependent membrane proteins, receptors and ion transport channels increases. Efficient transport of ions is an extremely important factor in the high performance and stability of body cells.

8. Stabilization of cell and subcellular membranes of all organs and tissues, with the exception of lymphoid. Thus, under the influence of HA, cells become more resistant to alteration.

9. Strengthening the detoxification function of the liver. GCs increase the activity of a number of hepatic enzymes, as a result of which the detoxifying function of the liver increases.

10. Increased migration of eosinophils from the bloodstream to tissues, where they actively perform the functions of phagocytes, bind and break down excess biologically active substances, in particular, histamine. In addition, eosinophils are a source of kininases that destroy excess kinins.

However, the stress response is not only a way to achieve resistance. In some cases, it is possible to transform the reaction of adaptation into a reaction of maladaptation, damage, when the stress reaction contributes to the development of diseases, the so-called "diseases of adaptation", according to G. Selye. The disease will be the price that the body pays for the fight against the factors that cause stress. Adaptation diseases are diseases resulting from the imperfection of the OSA mechanisms, its relative expediency, it is the result of either an insufficient stress response or a prolonged and pronounced hyperfunction of stress mechanisms. According to G. Selye, the disease is a state of life that has come out of the limits of adaptation. The disease does not occur if the body has well-developed adaptive mechanisms. The condition for the onset of the disease and its serious course are, according to G. Selye, “deficiency of adaptive energy, depletion of defense mechanisms”

The transition of a stress reaction into its opposite occurs if it is excessively strong, very long, often repetitive, or if the adaptive mechanisms of the body are initially weak.

Why does the stress syndrome, this inherently protective reaction, lead to the depletion of the adaptive potential? What are the adverse stress factors?

Among the unfavorable stress factors, first of all, should be attributed the unusually long-term effect of high doses of GCs and CHs. During stress, the concentration of CH in the blood can increase by 20-50 times or more. With their action, the occurrence of ulcerative lesions of the stomach during severe stress is largely associated. Ulcerative lesions of the stomach under a variety of stressful effects occur with such great constancy that they are considered obligatory sign stress syndrome. Hans Selye described the triad of changes characteristic of any marked stress. These three main changes under stress, along with hypertrophy of the adrenal cortex, involution of the thymicolymphatic apparatus, include the formation of ulcers in the gastrointestinal tract.

High concentrations of CH and HA lead to spasm of the arterioles of the muscular layer of the stomach. Vasospasm entails stasis and subsequent hemorrhage into the mucosa or submucosa. As a result of ischemic damage to the mucosa and hemorrhages, focal necrosis develops in it, followed by ulceration. Ulceration is facilitated by an increase in the acid-peptic factor and a decrease in the production of protective mucus under the influence of HA.

The development of stress damage to the myocardium is also associated with the action of high concentrations of CH. Large doses of norepinephrine cause an increase in the entry of Ca2+ ions into myocardial cells, the excess of which, in combination with an excess of free fatty acids, due to the activation of catecholamine-dependent lipolysis, leads to swelling of mitochondria, uncoupling of oxidative phosphorylation and a deficiency of ATP and creatine phosphate in myocardial cells. At the same time, calcium overload causes contracture contractions of myofibrils, as this disrupts the phase of diastolic relaxation. This energy-deficient situation and contracture eventually lead to small-focal necrobiotic changes in the myocardium. Stress hypokalemia also contributes to stress damage to the myocardium.

Calcium overload, which occurs with an excessively strong or prolonged stress reaction, has a toxic effect not only on cardiomyocytes, but is a universal mechanism of cell damage. Thus, calcium overload of cells can become one of the unfavorable stress factors.

Excessive intensification of lipid peroxidation (free radical) oxidation of lipids (LPO) is also associated with the action of high concentrations of catecholamines. Under the influence of LPO products - lipid hydroperoxides - the formation of free radicals, labilization of lysosomes, release of proteolytic enzymes occur, and as a result, highly toxic products appear - aldehydes, ketones, alcohols, the accumulation of which causes damage to membrane-bound enzymes, disruption membrane transport and cell death. There is every reason to state that LPO activation under stress is a universal mechanism of cell death and plays the role of a key pathogenetic link in damage to various organs and tissues. The significant role of lipid peroxidation in the pathogenesis of stress damage is confirmed by the positive effect of antioxidant drugs on the function and structure of cells. A particularly protective effect of antioxidants was noted during stress damage to cardiomyocytes (Petrovich Yu.A., Gutkin D.V., 1986; Baraboy V.A. et al., 1992)

Prolonged hyperlipidemia is another unfavorable stress factor. Under stress, the mobilization of fat from the fat depot is increased. Activation of lipolysis leads to the formation of free fatty acids - energy donors for intensively functioning organs. However, the use of fatty acids is associated with an increase in oxygen consumption. With its deficiency under the action of a stress factor, the utilization of free fatty acids is disturbed, their accumulation occurs, initiating a number of pathological processes: fatty degeneration of the liver, increased blood clotting and vascular thrombosis, development of atherosclerosis, hypertension. In addition, the stress response is characterized by the activation of phospholipases, which is accompanied by the redistribution of phospholipids, the formation of lysophospholipids with detergent properties. As a result, the structural organization, phospholipid and fatty acid composition of the lipid layer of membranes change, the lipid environment of membrane-bound proteins that act as enzymes and receptors changes. These moderate changes increase the activity of these proteins. However, with an excessively long and intense stress response, excessive activation of phospholipases leads to damage to cell membranes, to inactivation of membrane-bound cell receptors, ion channels, and pumps.

Prolonged hyperproduction of HA may be accompanied by severe atrophy of the lymphoid tissue. Since the lymphoid tissue is the basis of the immune system, the result of its atrophy should be the insufficiency of immune defense mechanisms, a decrease in the effectiveness of immune surveillance, which facilitates the malignant transformation of cells.

Another result of excessive production of HA is the suppression of the inflammatory response. As you know, inflammation is a kind of barrier that prevents the further spread of an infectious agent outside the zone of introduction. GCs, which have an anti-inflammatory effect, by suppressing inflammation, thereby inhibit this barrier and contribute to the spread of infection. It has long been noted in the clinic that prolonged stress predisposes to the exacerbation of chronic infectious diseases or contributes to the emergence of new infections.

The stress response is also characterized by the activation of proteolytic systems, which leads to the denaturation of protein structures. Under stress, in contrast to inflammation, there is not a sufficient increase in the content of proteolysis inhibitors, which, for example, during inflammation are acute phase proteins.

Thus, under certain conditions, the stress response can turn from a link in the body's adaptation to various factors into a link in the pathogenesis of various diseases. At present, the role of stress as the main etiological factor in ulcerative lesions of the gastric mucosa and duodenal ulcer, coronary heart disease, hypertension, and atherosclerosis has been shown. Stress, especially chronic, also contributes to the development of immunodeficiency states, autoimmune diseases, neurosis, impotence, infertility, cancer, etc. (P.D. Horizons, 1981; F.I. Furdui, 1981; V.A. Evseev, Magaeva S.V., 1985; Kryzhanovsky G.N., 1985; 1985)

After all of the above, the following questions will be legitimate: “What is stress? Is stress good or bad? Is stress physiological or pathological? Stress is still a biological defense phenomenon aimed at increasing the body's resistance to stimuli, although it includes elements of damage. Life is impossible without stress. G. Selye wrote that complete freedom from stress means death. Stress is not adverse life circumstances, but a defensive reaction to these circumstances, while stress may not cause any harm to the body. Stress does not necessarily and not in every case lead to pathological phenomena. G. Selye himself proposed to distinguish between 2 types of stress - eustress and distress (English distress - exhaustion, misfortune). Eustress is physiological stress, adaptive, it mobilizes and trains the body's defense resources without harming it. Distress is a pathological, harmful or unpleasant stress that leads to the development of pathology. It is distress that serves as the pathogenetic basis for the development of diseases - diseases of adaptation, according to G. Selye (G. Selye, 1979)

A person has a number of mechanisms that prevent excessive activation of the stress system and, accordingly, the implementation of the damaging effects of excessive concentrations of stress hormones. These are the so-called stress-limiting mechanisms (Meyerson FZ, 1986). The intensity of the stress reaction is precisely determined by the ratio of the degree of stimulation of stress-realizing mechanisms under the action of a stressor on the body and the activation of stress-limiting factors.

Stress-limiting systems can be divided into central ones, the main task of which is to limit and activate the central links of the stress system, and peripheral ones, whose action is aimed at increasing the resistance of cellular structures and organs to damage.

Restriction of the activity of stress-realizing mechanisms is primarily achieved by increasing the release of central inhibitory mediators, such as dopamine, serotonin, glycine, and, especially, -amino-butyric acid. (Meyerson F. Z., 1980). -aminobutyric acid (GABA) is the main inhibitory mediator in the central nervous system, synthesized in the brain by decarboxylation of glutamate (Roberts cycle). CA, accumulating in excessive concentrations, block the natural pathways of metabolism of -ketoglutaric and succinic acids in the Krebs cycle, which leads to the activation of an alternative pathway for their use. As a result, the formation of GABA increases sharply. The anti-stress effect of the GABAergic system is realized at the level of the higher vegetative centers of the brain and consists in preventing excessive release of cortico-liberin and catecholamines. The inhibitory effect of GABA on the catecholamine link of the stress system is carried out not only in the CNS, but also in the periphery, limiting the release of CH from sympathetic neurons innervating organs and tissues.

One of the metabolites of the GABAergic system, -hydroxybutyric acid, which, unlike GABA, penetrates well through the blood-brain barrier when introduced into the body from the outside, is already used to prevent stress damage to various organs, in particular, to prevent further damage to the heart muscle in myocardial infarction.

Another central stress-limiting factor is the opioid system. (Ignatov Yu.D., 1982; Limansky Yu.P., 1983; Pshennikova M.G., 1987) Under stress, there is an increase in the synthesis and release of endogenous opioid neuropeptides, which are currently divided into three groups: proenkephalin, represented mainly by leu- and methenkephalins, propiomelanocortinic, -endorphin has the greatest physiological significance from this group, and prodynorphin, which includes dynorphin A, dynorphin B, or leumorphin, as well as - and -neoendorphins. These neuropeptides have a pronounced sedative effect, increase the sensitivity threshold for pain stimuli, have the ability to suppress the production of pituitary stress hormones, limit the excessive activity of the sympathetic-adrenal system, thereby preventing catecholamine-mediated damage in the body. Limitation of the effects of the sympathetic system is also carried out by inhibiting the release of norepinephrine from sympathetic nerve endings through opiate receptors. This result is achieved due to the inhibition of adenylate cyclase by opiates and, for this reason, a decrease in Ca2+ transport into presynaptic membranes. The analgesic effect of opioid peptides is largely realized due to the ability of the latter to increase the activity of the serotonergic system. One of the consequences of the activation of the serotonergic system is the blockade at the level of the spinal cord of the conduction of nociceptive impulses from the primary afferents to the overlying sections of the CNS.

In recent years, data have been obtained that the NO system is involved in the regulation of the stress response, preventing its excessive activation, affecting both its central and peripheral links (Malyshev I.Yu., Manukhina E.B. ,1998) It was found that under stress caused by the action various factors, there is an increase in the synthesis of nitric oxide, which is able to limit the release of pituitary stress hormones, block the release of catecholamines from the adrenal glands and sympathetic nerve endings. In addition, with the participation of NO-dependent mechanisms, some peripheral stress-limiting mechanisms are realized. It turned out that nitric oxide is able to limit damage during the stress response by suppressing free radical oxidation by increasing the activity of antioxidant enzymes and enhancing the expression of genes encoding them. In addition, nitric oxide itself has antioxidant properties. It was also found that NO activates the synthesis of cytoprotective heat shock proteins, or stress proteins, which are known to be an important system for protecting cells from stress damage. Nitric oxide, along with group E prostaglandins and prostacyclin, plays an important role in preventing platelet adhesion and aggregation, which may determine its protective effect during stress activation of thrombus formation.

Peripheral stress-limiting mechanisms include the prostaglandin, antioxidant systems, and the system of protective heat shock stress proteins.

The prostaglandin system includes the prostaglandins themselves, especially the E and I2 group prostaglandins, and their receptors. Prostaglandins belong to the group - eicosanoids, derivatives of arachidonic acid.

The protective effect of PGE under stressful influences is determined by their three main properties: the ability to suppress the release of catecholamines from sympathetic nerve endings, to have a vasodilator and direct cytoprotective effect (Pshennikova M.G., 1991) Prostaglandins of groups E and I2, the production of which increases with activation of the sympathetic-adrenal system, have the ability to block the release of norepinephrine from presynaptic membranes. As a result, the effect of CH on effector cells is limited, in particular, the stomach vessels are protected from adrenergic spasms during stressful situations (Fuder H., 1985) In a number of organs and tissues (adipose tissue, stomach), PGE inhibit the formation of cAMP upon stimulation -adrenergic receptors. Thus, catecholamine-dependent lipolysis is inhibited and the release of free fatty acids into the blood decreases.

PGE, and especially PGI2, have pronounced vasodilator properties. The action of PGI2 is most effective in relation to the small arteries of the coronary bed. Being synthesized in the endothelium of these vessels, it acts as a powerful coronary dilator (Moncada S., Vane J.R., 1979).

PGI2 are effective antagonists of thromboxane A2, a powerful inducer of platelet aggregation and vasoconstrictor, as well as leukotrienes, which have a strong vasoconstrictive effect (Lefer A.M., 1986).

The cytoprotective effect of PGs is based on their direct stabilizing effect on cell membranes. PG can suppress lipid peroxidation and thereby prevent the damaging effect of lipid peroxidation products on cell membranes.

Another mechanism for limiting stress-induced damage is the activation of the synthesis of highly active protective heat shock stress proteins, which help the cell survive stressful situations. They are involved in the restoration, "repair" of damaged proteins that have acquired an incorrect conformation as a result of adverse effects. The name of these specific proteins is not entirely accurate. They got their name because they were first discovered in cells exposed to heat that exceeded the optimum temperature for the cell. Heat shock proteins are a system consisting of 4 groups of regulatory proteins with different molecular weights and functions. But common to all of them is that their synthesis increases dramatically in response to a variety of cell damage and that they increase the cell's resistance to damage, limit proteolysis, stabilize signal receptors, promote the work of the repair system, inducing programs that eliminate damage in cell or damaged cells themselves. Under stress conditions, heat shock proteins, interacting with steroid hormone receptors, can block the excessive effect of these hormones on cells.

An equally important factor in the natural prevention of stress damage is the antioxidant system, which directly protects cell membranes from the damaging effects of free radicals. The main elements of the body's defense against the action of toxic factors of oxygen metabolism are antioxidant enzymes - superoxide dismutase, catalase, glutathione peroxidase, which break down the main reactive oxygen species.

Other factors are also involved in protecting against reactive oxygen species in the body. First of all, these are non-enzymatic antioxidants - -tocopherol, vitamins of groups A, C, K, P, which are active against almost all free radicals.

Of the other agents, steroid hormones, bilirubin, ceruloplasmin (affecting free blood iron), transferrin, albumins, and SH-groups of proteins have antioxidant activity.

Stimulation of the antioxidant defense mechanisms of the body contributes to the limitation of free radical oxidation during stress.

Thus, the development of the general adaptation syndrome and its outcome depend on the degree of manifestation of stress-realizing and stress-limiting systems and the nature of their interaction. Experimental and clinical studies have shown that the use of GHB, synthetic opiates, serotonin, -tocopherol, antioxidants, benzodiazepine derivatives (phenozepam), which potentiate the effects of the GABA system at all levels of the CNS, can reduce the damaging effect of the stress response during congenital or acquired inferiority of stress-limiting factors.

333. Baraboy V.A., Brekhman I.I., Golotin V.G., Kudryashov Yu.B. Peroxidation and stress. SPb., 1992.

334. Horizons P.D. //Vestn. USSR Academy of Medical Sciences - 1979.- N 11.- S.12-18.

335. Horizons P.D. Stress // Homeostasis.- M., 1981.- S.538-570.

336. Gushchin I.S. //West. USSR Academy of Medical Sciences - 1985.-N 8.- P.63-65.

337. Evseev V.A., Magaeva S.V. //Vestn. USSR Academy of Medical Sciences - 1985.-N 8. - P.18

338. Ignatov Yu.D. /Pharmacology of neuropeptides. - M., 1982.- S. 742

339. Zaichik A.Sh., Churilov A.P. General pathophysiology. T.1. - St. Petersburg, 2001.

340. Kryzhanovsky G.N. //Vestn. USSR AMS. - 1985.-N 8.- S. 3-12.

341. Laycock J.F., Weiss P.G. Fundamentals of endocrinology. - M., 2000.

342. Limansky Yu.P. // Pharmacological aspects of anesthesia.-L., 1983.-S. 22-28.

343. Malyshev I.Yu., Manukhina E.B. //Biochemistry, - 1998.- T. 63, no. 7.- S.992-1006.

344. Meyerson F.Z. // Patol. fiziol, and experiment. therapy. - 1980.- N 5.- S.3-16.

345. Meerson FZ //Physiology of adaptation processes. -M., 1986.- S.521-631.

346. Mechanisms of development of stress /Under the general editorship of F.I. Furudui-Kishinev, 1987.

347. Petrovich Yu.A., Gutkin D.V. // Patol. physiol. and experiment. therapy. 1986, - N 5.-S.85-92.

348. Pshenniekova M.G. // Patol. physiol. and experiment. therapy. - 1987.- N 3.-S.85-90.

349. Pshennikova M.G. // Patol. physiol. and experiment. therapy. - 1991.- N 6.-S.54-58.

350. Pshennikova M.G. // Patol. physiol. and experiment. therapy. - 1991.- N 6.- S.54-58.

351. Selye G. Essays on the adaptation syndrome. - M., 1960.

352. Selye G. Stress without distress. - M., 1979.

353. Sudakov K.V. // Patol. physiol. and experiment. therapy. - 1992. - N 4.- P.86-93.

354. Tigranyan R.A., Vakulina O.P.//Space biol.-1984.-N 6.- C 83

355. Tigranyan R.A. Stress and its importance for the body. - M., 1988.

356. Tolyanina V.G. // Physiological journal. -1997.- N 4.- S.9-14.

357. Fuder H. //J. cardiovascul. Pharmacol.-1985/-Vol. 7, -N 5-P.52-57.

358. Moncada S., Vane J.R. //pharmacol. Rew.-1979-Vol. 30.-P.293-331.

359. Lefer A.M. //Biochem. Pharmacol.-1986.-Vol.35.-P.123-127.

March 1 - May 31, 2018 The Russian Academy of Natural Sciences (International Association of Scientists, Teachers and Specialists) and the editors of the journals "Start in Science", "International School Scientific Bulletin" held the V International Competition of Research and Creative Works of Students "Start in Science".

21 – 24 May 2018 scientific events of the RANH took place in Moscow: International scientific conference " Topical issues Science and Education”, International Scientific Conference “Innovative Medical Technologies”, XXIV Scientific and Practical Conference “International Certification Systems for Scientific and Pedagogical Personnel”, XXXVII International Exhibition and Presentation of Educational and Methodological Publications.

The Academy of Natural Sciences took part in one of the largest scientific and educational forums in Russia.

March 16-19, 2018 The Russian Academy of Natural Sciences took part in the 38th International Paris Book Fair LIVRE PARIS

February 27-28, 2018 RANH scientific events were held in Moscow: Final meeting of teachers of higher and secondary schools, International scientific conference "Modern problems of science and education", International scientific conference "Innovative medical technologies", Scientific and practical conference "International certification systems for scientific and pedagogical personnel" , XXXVI International exhibition-presentation of educational and methodical publications.

Born in 1907 in the family of a doctor in Austria-Hungary. After graduating from the Medical Faculty of the University of Prague, he continued his studies in Rome and Paris. With the coming to power of the fascists, the scientist anti-fascist emigrated to Canada, which became his second home. There he finally took shape as a scientist, headed the Institute of Experimental Medicine and Surgery (now the International Institute of Stress), gained worldwide fame for his work on the problem of stress. Hans Selye repeatedly visited Russia, in 1935 he met with I. Pavlov, about whom he retained the warmest memories. As Hans Selye himself later wrote, "Conversations with him inspired me throughout my life." He is the author of many works, many of which have been translated into Russian. The book "Essays on the Adaptation Syndrome" has acquired the greatest fame. Even at the dawn of his scientific activity, G. Selye drew attention to the fact that many infectious diseases caused by completely different pathogens that have their own, different from others, clinical picture, at the very beginning show identical symptoms (fever, general weakness, loss of appetite) . Only after some time, symptoms appear that are specific to a particular disease, allowing them to be differentiated and a correct diagnosis to be established. To be more precise, this fact was noticed by many. The merit of Hans Selye was that he looked at it in an innovative way, explained it differently. He put forward and later brilliantly proved the hypothesis of a general adaptation syndrome, from which he moved on to the universal concept of stress. At the beginning of a number of diseases, patients experience general discomfort, what is called "uncomfortable." Then there is weakness, irritability, in children - tearfulness. With infectious diseases, the temperature rises. All these signs speak of some still incomprehensible painful manifestations, of a non-specific, uniform protective reaction of the body, which G. Selye called the general adaptation syndrome. And only then, when other symptoms join (rash on the body, indigestion, pain in certain parts of the body, etc.), we can talk about the diagnosis, about the specificity of the symptoms of the disease. The most interesting next. In the development of the adaptation syndrome, three stages are distinguished: the alarm reaction, the phase of resistance and the phase of exhaustion. In the first, the organism begins, though rather timidly, to resist the changed conditions of existence or adapts to them. In the phase of resistance, adaptation to new conditions is carried out, the body is fully opposed to the effects of the stressor. In the third phase, which occurs after prolonged exposure to a stressor, all adaptation reserves come to an end, and the organism dies. Naturally, the last phase does not always develop. In most cases, the body copes with the stressor in the first or second phases of the general adaptation syndrome. What is the underlying mechanism of the syndrome? The first place belongs to the hypothalamus-pituitary-adrenal cortex system. We will not go into details of the operation of this system. Let's just say that the end product of her work is the hormones of the adrenal cortex (corticoids). It is they who play the leading role in organizing resistance to the stressor. Their concentration in the blood increases dramatically under the influence of a stressor, and the outcome of the struggle largely depends on whether they are enough. The stage of exhaustion is characterized by the sharpest inhibition of the functions of the adrenal cortex.

Outstanding physiologist of the XX century. G. Selye in the mid-50s developed a concept according to which adaptation has two components - specific and non-specific. A specific component is specific adaptations of specific organs, systems, biochemical mechanisms that ensure the most efficient operation of the whole organism in given specific conditions. For example, in mountainous regions, where the oxygen content in the atmospheric air is lower than at sea level, there are a number of features of the blood system, in particular, an increased concentration of hemoglobin (so that oxygen can be more efficiently extracted from the air passing through the lungs). The appearance of pigmentation (sunburn) on the skin in people who have been under conditions of strong insolation (solar radiation) for quite a long time is also an example of structural specific adaptation that reduces the risk of damage by excess radiant energy to those tissues that are located below the surface layers of the skin. There are many such examples, and they have been well known for a long time. Specific adaptations in the body are formed due to a change in the activity of certain parts of the genome in those cells on which such an adaptation depends, and this occurs over a fairly long time. Usually a person needs 6-8 weeks to fully adapt to the effects of a new factor for him.

Specific adaptations are divided into phenotypic (individual), developing during ontogenesis (individual development of the organism) of each individual, and genotypic, or inherited. In addition, two stages are distinguished in phenotypic adaptation: urgent and long-term.

The main merit of G. Selye is that he drew attention to the non-specific components of adaptation, which are always revealed, regardless of the nature of the acting factor. Selye was also able to understand the basic mechanisms hormonal regulation, formed in the initial period of adaptation, called the stress response. need adaptive stressful self-diagnosis

Hans Selye wrote that the process of adaptation is associated with the formation of the General Adaptation Syndrome (GAS). Reactions to stressful influences are pathological only under certain conditions, but in principle they have an adaptive value, and therefore they were called by Selye the "general adaptation syndrome". General adaptation syndrome - a complex of reactions that occurs in the whole organism under the influence of various damaging factors and ensures the adaptation of the organism to given conditions. In later works, he combined the terms "stress" and "general adaptation syndrome" and used them as synonyms (Selye) (1982).

The classic general adaptation syndrome was described in 1936 by G. Selye as a process consisting of three successive stages.

• 1. The alarm stage (alarm reaction), in turn, is characterized by two phases: the shock phase and the countercurrent phase. With a significant stressor, the stage of anxiety can end in the death of the organism.
• - increased release of adrenaline into the blood, which ensures the mobilization of carbohydrate and fat resources for energy purposes and activates the activity of the insular apparatus β-cells, followed by an increase in the content of insulin in the blood;
• - increased release of secretory products into the blood by cortical cells, leading to the depletion of their reserves of ascorbic acid, fats and cholesterol;
• - decreased activity of the thyroid and gonads
• - weight loss
• 2. If the organism survives this essentially protective stage of the syndrome, the resistance stage begins.
• - accumulation in the adrenal cortex of precursors of steroid hormones (lipoids, cholesterol, ascorbic acid) and increased secretion of hormonal products into the bloodstream;
• - activation of synthetic processes in tissues with subsequent restoration of the normal weight of the body and its individual organs;
• - further reduction of the thymic-lymphatic apparatus;
• - a decrease in insulin in the blood, providing an increase in the metabolic effects of corticosteroids.
• 3. With prolonged action of the stressor, the previous one passes into the stage of exhaustion.

During the anxiety stage, the nonspecific resistance of the body increases, while it becomes more resistant to various influences. With the transition to the stage of resistance, nonspecific resistance decreases, but the body's resistance to the factor that caused stress increases.

The functional state is the level of activity of the organism at which one or another of its activities is performed. The lowest levels of the functional state are coma, then sleep. The highest level is aggressive-defensive behavior.

One of the varieties of functional states is stress. The doctrine of stress was created by the Canadian physiologist Hans Selye. Stress is a functional state with which the body responds to extreme influences that threaten its existence, its physical or mental health. Therefore, the main biological function of stress is the adaptation of the body to the action of a stressor or stressor. There are the following types of stressors:

• 1. Physiological. They have a direct effect on the body. These are pain, heat, cold and other stimuli.
• 2. Psychological. Verbal stimuli signaling current or future harmful effects.

According to the type of stressors, the following types of stress are distinguished:

• 1. Physiological.
• 2. Psychological.

a. information stress occurs during information overload, when a person does not have time to make the right decisions.

b. emotional stress. Occurs in situations of resentment, threats, dissatisfaction.

Selye called stress a general adaptation syndrome, since he believed that any stressor triggers non-specific adaptation mechanisms of the body.

3. Valeological methods of self-diagnosis

Evaluate your type of constitution: Pignet index, Chernorutsky method, calculation of ideal weight based on the Brock index and Quetelet index.

The Pinier index is an indicator that characterizes a person's body type. It is calculated on the basis of determining the ratio of height, weight and chest girth.

Calculation of the indicator:

The Pignet index is calculated using the following formula:

Pinier index = Height (cm) - Weight (kg) - Bust (cm)

Personal data:

Conclusion: based on the interpretation of the Pignet index, my body type is "weak".

Chernorutsky's technique.

The Chernorutsky scheme is often used as a technique for predicting the likelihood of obesity. According to this scheme, weight in kg and chest circumference in cm must be subtracted from height in cm. In fact, the scheme was created in 1925 to determine the type of physique. In this capacity, it is still used - everyone knows the division of people into asthenics, normosthenics and hypersthenics.

Chernorutsky called persons with a large Pigne index as asthenics, with average values ​​- normosthenics, and with small values ​​- hypersthenics. Although in Chernorutsky's classification types are distinguished on the basis of morphological differences, characteristic physiological parameters were described for each type (BP, respiratory volumes, the nature of secretion and motility of the gastrointestinal tract, intestinal absorption capacity, functions of the endocrine glands, the amount of erythrocytes and hemoglobin in the peripheral blood) .

It is pointless to use the Chernorutsky scheme for diagnosing weight problems - according to it, only hypersthenics are at risk. This idea is not confirmed by modern statistics - it is known that obesity can threaten people of any physique.

Personal data

My Pignet index is 30

Based on the Chernorutsky method for determining the physique according to the Pigne index, we can conclude that my body type is “asthenic”

Calculation of ideal weight based on Broca's index and Quetelet's index

Broca's index

The ideal weight formula was developed in 1871 by the French surgeon and anthropologist Paul Broca. The formula is suitable for people above 155 and below 185 centimeters of average build. This is an updated definition for its first known form (growth minus 100):

Personal data:

My ideal weight = (167cm - 100) H 0.85 = 56.95

My weight is 52 kg, which is slightly below the ideal weight according to the Brock index.

Quetelet index

This method was developed by the famous Belgian sociologist and statistician Adolphe Quetelet in 1869. About 150 years have passed since then, and the technique is still the most popular for determining the state of weight of a person over 20 years old.

Body mass index (BMI) = body weight (in kg) / height (in m2)

Results processing:

Personal data:

My BMI = 52/(1.67)2 = 18.6 units

My Quetelet index is 18.6 units, which corresponds to a slight underweight