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Stress limiting factors

Since in every realizing factor of the general adaptation syndrome with its uncontrolled development there is a potential danger of the appearance of pathogenic transformations, there must be a natural system of control, self-limitation of these factors.

F.Z. Meerson and M.G. Pshennikova [16] note two significant features of the process of adaptation to stress situations. First, stress-realizing factors are included only when adaptation to changes in external conditions cannot be achieved only through external, behavioral reactions, and the stress response reproduces a physiological phenomenon equivalent to what in everyday life is designated as patience or endurance . Secondly, as the action of the external stimulus continues (if it does not exceed the individually determined possibilities of the stress reaction), the irritation of the stress-realizing factors gradually diminishes due to the achievement of the adaptation effect. providing a kind of “patience” of the organism at the physiological level. This is reflected in a decrease in blood concentration of catecholamines acting on target organs, and in reducing the likelihood of stress damage to internal organs.

In other words, the situation is reproduced in which stress-realizing factors acquire increased power up to a certain time and continue to work in accordance with this power, without experiencing the stimulating effect of the stress reaction on the continued influx of external stimuli. This situation is very beneficial for the body. Essentially, it is the basis of adaptation to stress. On this basis, the authors put forward a hypothesis [15], according to which one of the main mechanisms of adaptation to stress situations is the activation of central regulatory mechanisms that inhibit release of releasing factors and, as a consequence, the release of catecholamines and corticosterone. Such mechanisms are associated with various factors that provide both central and peripheral regulation of the developing stress reaction. They were designated by the authors as stress-limiting factors, or stress-limiting systems. It is logical to assume that in the process of evolution, the conjugation of stress-realizing and stress-limiting factors provides an increase in adaptive capacity for repeated stress effects. At the same time, an organism can be protected not only from damaging stress situations, but also from many damaging environmental factors, which are blocked by stress-limiting systems. This assumption was confirmed by special studies [15]. The use of short-term stressful effects or drugs, including metabolites of stress-limiting systems, contributed to the prevention and treatment of stressful injuries, as well as diseases pathogenetically associated with previous stress, such as duodenal ulcer or stomach ulcer, autoimmune or allergic diseases, ischemic heart disease, blast disease. diseases.

The authors identify several central stress-limiting factors, which are designated as individual stress-limiting systems. This is, firstly, the GABA-ergic system. Gamma-aminobutyric acid (GABA) is a mediator of postsynaptic inhibition of brain and spinal cord neurons and presympathic blockade of neurotransmitter release from various nerve terminals. The stress-limiting effect of the GABAergic system is due to the presence of GABAergic receptors and GABAergic CNS neurons in the innervation of almost all organs.

The action of the second stress-limiting system, the benzodiazepine, is closely related to GABA receptors. The natural and synthetic products of the benzodiazepine series are benzodiazepine (diazepam). phenozepam are classic ligands. They potentiate the effects of GABA systems at all levels of the central nervous system.

Third, the opioidergic system is represented in the body by opioid peptides and opioid receptors. Opioid peptides are endogenous products with analgesic morphine-like action. As established by studies of the last decade [17, 26], they are regulators and modulators of many processes, and the analgesic effect is just one of the manifestations of their complex function. Studies of a group of domestic immunologists under the guidance of R.V. Petrov in 1984 discovered previously unknown regulatory peptides of bone marrow origin, called myelopeptides [24]. They possess both opioid and immunomodulatory activity. These studies confirmed the complex polyfunctional and highly branched nature of the opioidergic system. Opioidergic receptors are located in cells of various parts of the brain, as well as in many organs and tissues, localized in synapses, nerve endings, on secretory cells and other effector cells. Stress response stimulates the formation of opioid peptides. Under stress, they contribute to an increase in the perception of pain and other irritants, as well as prevent severe hyperthermia.

Topographically and functionally, the opioidergic system is associated not only with stress-realizing factors, but also with other stress-limiting systems.
One of them is the serotonergic system. Opioid peptides cause intense naloxone-dependent release of serotonin from serotinergic neurons. On the other hand, the analgesic effect of opioid peptides is significantly potentiated by serotonin. It follows from this that congenital or acquired insufficiency of the opioid or serotonergic systems increases the body's vulnerability to stress effects [16].

Peripheral stress-limiting mechanisms are implemented through an antioxidant and antioxidant defense system, as well as through a prostaglandin system.

As you know, stress hormones (catecholamines, vasopressin, and others) increase the activity of lipases and phospholipases, which contribute to the intensification of POL. As a result, the viscosity decreases and the fluidity of the membrane lipid bilayer increases, which facilitates the mobilization of peptide bonds of active functional membrane-bound proteins. In a moderate, controlled degree, this process is a necessary component of the stress response. However, the uncontrolled intensification of lipid peroxidation contributes to the damage of various organs and tissues. An antioxidant defense system acts as a controlling factor, the production of active products of which increases along with the intensification of POL. The failure of this system increases the damaging effect of the stress response.

The prostaglandin system is represented by a series of compounds - derivatives of polyunsaturated fatty acids with 20 carbon atoms [5]. The main precursor of prostaglandins is arachidonic acid. The products of its metabolism (prostaglandins, thromboxane, prostacyclin, leukotrienes) are mediators and regulators of cell response to various external stimuli and generally have an important effect on cell growth and viability, on intracellular metabolism. They are among the most powerful local stress-limiting factors.

Experimental and clinical studies established. that the use of GABA, as well as opioid peptides. synthetic opiates. serotonin, alpha tocopherol. synthetic antioxidants. Adenosine derivatives are able to reduce the damaging effect of the stress response in the case of congenital or acquired inferiority of stress-limiting factors [16].

Thus, the development of a general adaptation syndrome and its outcome depend on a complex set of regulatory mechanisms, or otherwise - management tools. Each of these management tools is characterized by its own tasks and its own solutions. In general, they have a common goal - the achievement of adaptation. although at the level of deep, cellular and molecular processes, they can show inconsistency, leading to disorganization and hindering the achievement of a common goal. In this regard, there are three levels of regulation of the stress response. The first level is the central regulation. It is achieved by a physiologically deterministic change in the hormonal status of the organism, in which the pituitary – adrenal cortex system takes the leading role, as well as a significant increase in the tone of the sympathetic level of the autonomic nervous system. The second level is the regulation of the local transformation of visceral functions. Here, the leading regulatory tool is the meta-sympathetic autonomic nervous system, which, during the development of the stress reaction, combines two extremely important functions. On the one hand, it maintains and protects, from powerful sympathetic impulses, the stability of the oscillation mode of local basic metabolic processes, the preservation of which is an indispensable condition for a return from an urgent (unstable) to a long-term (stable) adaptation of the organism. On the other hand, it immediately after the cessation (or already in the process) of stress influence is included in the management of the coordinated development of very fragile, vulnerable initial mechanisms of long-term adaptation, protecting them from the effects of pronounced sympathetic hypertonia. Finally, the third level of regulation is already directly correlated with the intermolecular intercellular interaction during the development of the general adaptation syndrome. Here are very complex mechanisms of self-regulation. the effect of which depends on the state of unstable equilibrium between stress-realizing and stress-limiting factors in their individual, specific for a particular organism manifestation. In the case of the prevalence of stress-realizing tendencies, there is a danger of the development of pathological manifestations associated with the uncontrolled activation of the mechanisms of urgent adaptation after the cessation of the stimulus. If the equilibrium shifts towards stress-limiting factors, there is a danger of a decrease in the level of reactivity of the organism, precluding the possibility of the full development of the general adaptation syndrome.
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