COMPENSATORY PROCESSES

From Big Medical Encyclopedia

COMPENSATORY PROCESSES (Latin compensare to counterbalance, compensate) — important type of the adaptation reactions of an organism to damage which are expressed that bodies and systems, directly not victims of action of the damaging agent, undertake function of the damaged structures by replaceable hyperfunction or qualitatively changed function.

As a result of development To. items are to some extent liquidated the disturbances of functions caused by damage therefore To. items are one of factors recovery (see). An important role in recovery is played also by other adaptation reactions of an organism providing destruction or restriction of a disturbing factor — development antibodies (see), phagocytosis (see), inflammation (see), a temporary immobilization of bodies and systems — guarding braking (see), and also processes of regeneration (see. Regeneration, in pathology ) To. the item should not identify with all complex of reactions of the damaged organism; it is impossible to identify To. the item and with adaptation in general, i.e. with the diverse reactions providing interaction of a healthy or sick organism with the environment (see. Adaptation ).

To. items can be implemented at the cellular, organ, system, intersystem levels. So, at destruction of one of genomes of a polyploid cell intracellular compensation is implemented due to increase in synthesis of RNA in the escaped genomes. At destruction of a part of nephrons of a kidney owing to a nephrosclerosis intraorganic compensation happens because function of the escaped nephrons amplifies and they hypertrophy. During removal of a stomach or long disturbance of its function intrasystem compensation is to some extent provided with strengthening of secretory function of underlying departments of the alimentary system. Intersystem compensation is observed at many diseases, in particular at anemias when disturbance of process of a hemopoiesis, decrease in quantity of erythrocytes and ability of blood to transport oxygen the long time is compensated by increase in minute volume of heart that is provided with compensatory hyperfunction of heart and the blood circulatory system in general.

At damage of an organism process of compensation of functions is quite often connected with process of recovery of the damaged cells. So, after damage to result of beam influence, a hypoxia, intoxication there is a recovery reversibly of the damaged cells due to intracellular regeneration, and these cells undertake function is irreversible destroyed. Recovery and intracellular regeneration are important premises of further development To. item. Regeneration of the whole bodies at high-organized animals and the person is impossible whereas To. items are rather perfect and, being one of types of adaptation, proceed on the basis of its general patterns.

To. and. have two stages: stage urgent and stage of long-term compensation. So, e.g., at injury of the right hand of people immediately begins to use the left hand. This urgent compensation is very important in extreme situations, however it is obviously imperfect.

Further as a result of training and formation in a brain of system of the new structurally fixed temporary bonds the skills providing long-term compensation — rather perfect performance by the left hand of the operations which are usually carried out right develop.

After removal or switching off owing to patol, process of one kidney urgent compensation in the form of compensatory hyperfunction of the remained kidney is implemented. However, despite simultaneous inclusion in process of all nephrons and mobilization funkts, a reserve of the remained kidney, its excretory function during the first several days is less than function of two kidneys. Further the mass of this kidney and the nephrons forming it increases, develops a compensatory hypertrophy of body, as a result the cut function of one kidney begins to correspond to function of two kidneys, the body recovers the funkts, a reserve; there is rather perfect long-term compensation, edges if there are no additional damages, can remain during all life. Also compensation at switching off owing to patol proceeds. process or removal of any other pair body — a lung, an adrenal gland (see. Vicarious processes ). Similarly after removal of an upper half of a small bowel urgent compensation in the form of strengthening of secretion of a stomach and a pancreas and increase in juice of a pancreas of activity of trypsin, a lipase, amylase is implemented. After this compensatory hyperfunction of the ferruterous device of a stomach and excretory department of a pancreas their compensatory hypertrophy making a basis of steady long-term compensation develops.

Expressiveness of a stage of urgent compensation and dynamics of its transition to compensation long-term in many respects depend on that, damage of an organism how fast develops. So, during the developing of traumatic heart disease owing to a lead of the two-fold valve, an injury of heart, a heart attack of a papillary muscle, and also at an experimental aortostenosis there is urgent compensatory hyperfunction of heart. This phenomenon is implemented at the expense of the law of Starlinga (see. Starlinga law ) and positive inotropic action catecholamines (see). In the beginning it is not followed by a hypertrophy of a myocardium, but is complicated by a complex of the shifts characteristic of heart failure. Further in process of development of a hypertrophy of heart and increase in its power of the phenomenon of heart failure gradually are eliminated, urgent compensation is replaced by steady long-term. At patients with rheumatism, at Krom damage of the valve device of heart develops gradually and also gradually load of heart increases, hyperfunction of heart is expressed to a lesser extent, also the hypertrophy caused by it slowly develops. In this situation transition of urgent compensation to long-term will be dragged out in time and clinically its definition is complicated. It, however, does not change the general provision that formation of urgent, but insufficiently perfect compensation and its subsequent transition to steady long-term compensation is the general pattern of development To. item. Understanding of the nature To. the item provides, first, disclosure of the mechanism of formation of urgent compensation and, secondly, disclosure of the mechanism of transition of urgent compensation to long-term.

Formation of urgent compensatory processes

During the studying of urgent compensation should be meant that the destruction of structures of an organism caused by damage, and developing after this dysfunction eventually break constancy of internal environment of an organism, it homeostasis (see). Disturbance of a homeostasis also causes response of an organism. In this reaction it is necessary to distinguish: activation of the systems specifically responsible for compensation funkts, defect, and activation of the adrenergic and pituitary and adrenal systems which are nonspecific joining at any damage of an organism or at change of conditions of the environment.

So, e.g., at switching off of one lung lobe at a lung fever owing to a lack of oxygen and excess of carbonic acid of blood there is an irritation of chemoceptors of sinocarotid and aortal zones and directly respiratory and vasomotor centers of a myelencephalon. There is compensatory hyperfunction of the device of external respiration and blood circulation which is combined with the expressed activation of adrenergic and pituitary and adrenal systems i.e. with a syndrome stress (see).

An important contribution to studying of the mechanism of urgent compensation were researches of P. K. Anokhin who developed idea of a crucial role of the afferent alarm system (see. Afferent synthesis ) in formation functional systems (see), specifically compensating funkts, the defect caused by damage. As a result of studying To. the item at disturbance of motive functions and functions of internals P. K. Anokhin formulated several general principles characterizing process of formation funkts, the system compensating funkts, defect.

1. The principle of the alarm system of defect, on Krom arises the first push to «turning on» of the corresponding mechanisms K. item 2. The principle of the progressing mobilization of reserve compensatory mechanisms which allows to understand how the ratio of the factors rejecting function from datum level, and factors defining the sequence of turning on of mechanisms of compensation is established. 3. The principle of the return afferentation from consecutive stages of recovery of the broken functions. 4. The principle of the authorizing afferentation, according to Krom in a brain, and especially in bark, is fixed that last combination of excitement, edges defined success of recovery of function in peripheral body. 5. The principle of relative instability of the compensated function which allows to estimate durability of each final compensation.

These principles can be applicable to To. the item, developing at damage of various bodies. So, e.g., injury of the lower extremity causes disturbance of balance and walking. It involves change of the alarm system from receptors of a vestibular mechanism, proprioceptors of muscles, receptors of skin of extremities and a trunk, and also visual receptors (the principle of the alarm system of defect). As a result of processing of this information in c. the N of page function of certain motor centers and muscular groups changes so that to recover to some extent balance and to keep traficability, though in the changed look. In process of increase in a damage rate the alarm system about defect can accrue, and then in To. items are involved new areas of c. N of page and the muscular groups (the principle of the progressing mobilization of reserve compensatory mechanisms) corresponding to them. Further in process of effective compensation or elimination of the damage the structure of the afferent pulse flow coming to the highest parts of the nervous system will change, will be switched off respectively certain departments of this funkts, the systems which were earlier participating in implementation of compensatory activity or to join new components (the principle of the return afferentation of stages of recovery of the broken functions). Preservation after recovery of rather stable anatomic defect will have an effect a certain combination of an afferentation coming to the highest parts of the nervous system which on this basis will provide formation of a stable combination of temporary bonds and optimum compensation, i.e. the minimum lameness at this damage (the principle of the authorizing afferentation).

Similarly anemia and an oligemiya after blood loss lead to fabric hypoxias (see), edges is an irritant of chemoceptors, stretch receptors of sinocarotid and aortal zones and the bulbar centers. In response to this alarm system about funkts, defect there is an increase in minute volume of heart, vasoconstriction of abdominal organs and muscles; this important reaction reduces a syndrome of a hypoxia of vitals, but does not eliminate it up to the end. Impulsation from the volyumoretseptor localized in the field of the right auricle includes in structure compensating funkts, systems the following important link, namely the increased allocation supraoptic both paraventrikulyarny kernels and a back share of a hypophysis of antidiuretic hormone (vasopressin), and cortical substance of adrenal glands — Aldosteronum. These hormones block allocation from an organism of sodium and water; as a result the oligemiya is eliminated, the fabric hypoxia is eliminated partially (the principle of the progressing mobilization of reserve compensatory mechanisms).

The fabric hypoxia operating from the very beginning and not eliminated stimulates formation of erythropoetin which, in turn, stimulates an erythrocytopoiesis; as a result of regeneration of red blood anemia and its investigation — a hypoxia — are eliminated. Elimination of it funkts, defect leads to the termination of the strengthened impulsation from the listed receptor zones (the principle of the return afferentation about recovery of functions); compensating funkts, system, having played a role, it is liquidated.

Unlike recovery of mass of blood after blood loss, at the majority of injuries of a human body and the highest animals of a complete recovery of bodies does not occur therefore funkts, the system created at a stage of imperfect urgent compensation turns into reliable long-term. It is observed also at injury of pair internals, the valve device of heart, digestive organs.

Formation of long-term compensatory processes

Transformation of urgent compensation into long-term makes the key moment To. item; it consists in increase in the power compensating funkts, systems and is shown by development of a hypertrophy of bodies which carry out compensation of disturbances.

The phenomenon providing transition from urgent compensation to long-term consists that increase in function of cells of the compensating systems causes increase in speed of a transcription as the first shift RNA (see) on structural genes deoxyribonucleic acid (see) in cellular kernels. The increase in quantity of poly-ribosomes which resulted from this activation provides increase in synthesis of protein and formation of additional intracellular structures that is shown by a hypertrophy of cells.

The cellular regulatory mechanism connecting the level of function of a cell with its genetic device and by that providing formation of structural bases of long-term compensation, T. 3. Meerson defined as interrelation Between function and the genetic device of a cell. This interrelation as a necessary link of all long-term adaptation reactions, and in particular compensations, is observed at all levels of regulatory hierarchy of an organism. So, at a reeducation of animals, to-rogo the leading right paw shall «concede» the situation in process left, process of development of this skill is followed by activation of synthesis of RNA and protein in neurocytes of a certain area of a cerebral cortex where the corresponding temporary bonds and skills are formed.

At compensatory hyperfunction of heart, kidney, a hepatic lobe activation of synthesis nucleinic to - t and proteins also makes a basis of a hypertrophy of these bodies.

the Diffraction pattern of neuron at its hyperfunction: disperse eukhromatiya, located in a body of a kernel (1), RNA what considerable accumulation of grains of silver testifies to (are specified by shooters) over a body of a kernel after introduction of the predecessor of RNA-uridine 5H3 intensively synthesizes; the condensed heterochromatin (2) connected with a kernel is inactive — over it grains of silver are absent; 3 — a kernel of neuron; 4 — cytoplasm; x 30 000.

It is essential that in the course of any long-term adaptation, in particular in the course of compensation, activation of synthesis nucleinic to - t and proteins is implemented not only in cells of one executive body on which the increased loading falls, but this activation develops and leads to emergence of certain structural changes in all links compensating funkts, systems, i.e. to development of the so-called system structural trace making a basis of long-term compensation. So, at the inborn heart diseases which are followed by the expressed hypoxia in addition to a hypertrophy of a myocardium, there is an activation of synthesis nucleinic to - t and proteins in marrow; as a result the expressed polycythemia provides increase in oxygen capacity of blood; in muscles formation of mitochondrions also increases and respectively their ability to absorb oxygen from blood increases. During the loss of the right hand the system structural trace is expressed by formation of the new bonds in a cerebral cortex providing performance by the left hand of the skills which are usually carried out right, a hypertrophy of the motive neurocytes innervating the remained extremity and a hypertrophy of her muscles, and also changes in bones of a shoulder girdle. Set of these structural changes created at the different levels forms the system structural trace making a basis of compensation. The changes developing in cells during the formation of a system structural trace were confirmed with D. S. Sarkisov, A. A. Paltsin, B. V. Vtyurin (1975) researches which by method of an electronic and microscopic autoradiography showed activation of the genetic device of cells of mammals at increase in their function. Most accurately this phenomenon is expressed at activation of synthesis of ribosomal RNA on the multiple genes localized in the nucleolar device of cells (fig).

It is obvious that at various damages compensating funkts, the system and the system structural trace forming in it have various architecture. At damage of a nervous system and the subsequent compensation of motive and intellectual disturbances this architecture is most difficult; at switching off of separate internals it is rather simple. However in all cases a key link of the forming system structural trace is the interrelation between function and the genetic device of a cell.

The mechanism of activation of the genetic device at hyperfunction of a cell became a subject of detailed researches. The compensatory hyperfunction arising at the first stage after damage of a cell naturally increases a consumption of ATP in cells of the compensating system, and on a nek-swarm short time resynthesis of ATP lags behind its expense. This temporary disturbance of the energy balance involves decrease in concentration vysokoergichesky connections (see) and increase in concentration of products of their disintegration. The size of the relation increases:

([ADF] • [creatine] • [phosphate inorganic]) / ([ATP] • [creatine phosphate]),

where in numerator — concentration of decomposition products of phosphoric connections, and in a denominator — concentration of these connections.

Change of concentration of these substances via the known mechanism of interface of oxidation with phosphorylation (see) influences resynthesis of ATP in mitochondrions.

At hyperfunction decrease in concentration of vysokoergichesky connections involves strengthening of oxidizing resynthesis of ATP in mitochondrions; at the same time concentration of creatine phosphate and ATP cease to decrease and are stabilized at the certain, a little reduced in comparison with norm level; power ensuring urgent compensation is as a result reached. However this compensation at reduced concentration of vysokoergichesky connections is unreliable since any additional loading can lead to disturbance of the unstable energy balance of cells and systems in general. The subsequent development of process is caused by the fact that decrease in concentration of vysokoergichesky connections influences not only oxidizing resynthesis of ATP, but through system of specialized intracellular mechanisms regulates activity of the genetic device of a cell. The decrease in concentration of ATP caused by hyperfunction activates synthesis nucleinic to - t and proteins and leads to increase in mass of structures. At the same time first of all the mass of mitochondrions increases, i.e. the power of system where there is a resynthesis of ATP increases. As a result concentration of ATP and creatine phosphate approaches datum level, synthesis nucleinic to - t and proteins in the increased mass of cells also approaches datum level — steady long-term compensation is established. The mechanism of self-control, by means of to-rogo deficit of energy is eliminated due to activation of the genetic device of a cell and formation of mitochondrions, is presented on the scheme 1.

Scheme 1. Intracellular link of compensation. Damage via the highest regulatory mechanisms causes hyperfunction of body. The mechanism of self-control in a cell can be presented as follows: hyperfunction of cells of body leads to increase in use of creatine phosphate and ATP. The attitude of concentration of decomposition products of creatine phosphate and ATP towards concentration of these connections (designated as the regulator of phosphorylation — the Russian Federation) increases; the increased size Russian Federation activates breath and the oxidizing phosphorylation of mitochondrions (a dotted contour of I) interfaced to it. The increased resynthesis of ATP stops further decrease in concentration of ATP in a cell — urgent compensation is secure. Further the increased size Russian Federation, working indirectly through a factor regulator (intermediate link), activates the genetic device of a cell, increases the speed of a transcription of RNA and by that causes growth of cellular structures. The compensatory hypertrophy — a basis of steady long-term compensation (a dotted contour of II) develops.

The main moment of urgent and long-term compensation consists that the same Russian Federation parameter puts another in action, more difficult, the mechanism of regulation indirectly — through a nek-swarm the intermediate link designated on the scheme as a factor regulator which controls activity of the genetic device of a cell determines the speed of synthesis nucleinic to - t and proteins. Therefore, at hyperfunction the increased size Russian Federation through a factor regulator activates synthesis nucleinic to - t and proteins, growth of intracellular structures results, compensatory develops hypertrophy (see) or a hyperplasia of cells (see. Hyperplasia ). Depression of function and the sizes Russian Federation involves opposite result — an atrophy from inaction.

The reality of this mechanism of regulation was for the first time proved in relation to compensatory hyperfunction and a hypertrophy of heart, and the following basic facts were determined. 1. Significant increase in function of heart naturally is followed by decrease in concentration of ATP and in a bigger measure of creatine phosphate. After this shift the speed of synthesis nucleinic to - t and proteins increases in a myocardium and its weight (hypertrophy) increases. 2. Increase in load of the heart which did not cause noticeable decrease in concentration of ATP and creatine phosphate does not lead to noticeable increase of speed of synthesis nucleinic to - t and proteins. 3. Any factor which is not increasing load of heart, but reducing concentration of ATP and creatine phosphate naturally causes increase of synthesis nucleinic to - t, proteins and as a result a hypertrophy of heart. Such factors are: ischemia of heart; the dissociation of oxidation with phosphorylation caused by cold or Isoproterenolum; and also genetic inferiority of mitochondrions at hereditary cardiomyopathies. 4. In culture of myoblasts the undervoltage of oxygen which is followed by reduction of content of ATP and creatine phosphate naturally involves increase of synthesis nucleinic to - t and proteins. 5. Increase in content of ATP and creatine phosphate naturally involves reduction in the rate of synthesis nucleinic to - t and proteins in myocytes of a cardiac muscle. This effect is reproduced by means of a hyperoxia in culture of myoblasts and develops also in the whole organism after switching off of a parasympathetic innervation. In the latter case disturbance of utilization of ATP and increase in its concentration in a myocardium naturally is followed by reduction in the rate of synthesis of RNA and proteins and a degrowth of heart. These facts demonstrate that the size Russian Federation defines not only synthesis of ATP, but also activity of the genetic device of a cell, i.e. formation of cellular structures.

Further it was shown that such communication between function and the genetic device — a key link of long-term compensation — is not exclusive accessory of heart. Role of deficit of energy in activation of the genetic device and first-priority increase in mass of mitochondrions in the course of compensation are established in cells of the most different fabrics now — in skeletal muscles, in neurocytes, in cells of a kidney, adrenal glands, etc.

The size Russian Federation exerts impact on the genetic device of a cell not in itself, and indirectly, via specialized mechanisms of cellular regulation. In this process an important role is played as intermediary metabolites of cyclic AMF by aliphatic polyamines, ions of magnesium; action of these metabolites is implemented through system of regulatory proteins of a cellular kernel.

The interrelation of function and the genetic device of a cell is implemented in all links compensating funkts, systems, formation of a system structural trace which increases the power of this system provides, and elimination or reduction caused by damage funkts, defect results.

In addition to the systems specifically responsible for elimination funkts, defect, at any damage adrenergic and pituitary and adrenal systems are activated, there is a generalized syndrome of a stress which makes a nonspecific component of any adaptation reaction, and compensatory reaction in particular.

A role of a syndrome of a stress

the Role of a syndrome of a stress in the mechanism K. the item it is caused by two important lines.

1. The general adaptation syndrome (see) includes considerable excitement of the highest vegetative centers and as a result activation of adrenergic and pituitary and adrenal systems. High concentration are as a result created catecholamines (see) and glucocorticoid hormones (see). At the same time, as P. D. Gorizontov showed, power and structural reserves of an organism will be mobilized.

Catecholamines increase the minute volume of heart, cause mobilization of a glycogen of a liver and a hyperglycemia, a lipolysis and increase in contents fat to - t in blood and respectively increase inflow of oxygen and substrates of oxidation to fabrics. Glucocorticoids, operating on genetic level, activate a gluconeogenesis and transamination and by that transformation of amino acids to glucose — a structural reserve of an organism in power. The stress caused by any factor of the environment is generalized reaction of the mobilization covering all organism.

2. Mobilization of energy and structural resources at a stress is combined with other, not less important phenomenon, namely with transfer of both power, and structural resources from the most various fabrics and systems in the systems responsible for adaptation to this specific environmental factor. So, ready condition to fight, and especially the fight, is characterized at animals not only the general mobilization of breath, blood circulation, a hyperglycemia, increase in contents fat to - t in blood, but also considerable vasoconstriction of abdominal organs and inactive muscles at simultaneous vasodilatation of active muscles.

Similarly in the nearest future after damage the excitement of adrenergic system inherent to a stress is combined with the expressed hyperemia in the bodies which are directly carrying out compensatory hyperfunction. Such hyperemia which is quite often followed by hemorrhages is observed in an initial stage of a compensatory hypertrophy of heart, only kidney, lung. These facts demonstrate that in the course of reaction of mobilization the increased amount of oxygen, glucose, fat to - the t selectively goes to the systems which are carrying out the increased function.

The catabolic effect of the increased concentration of glucocorticoids during a stress consists that in muscular, connecting, fatty tissue and in skin these hormones slow down synthesis of protein and nucleinic to - t and activate an albuminolysis; the amount of free amino acids considerably increases in a result in of blood. Against the background of this generalized catabolic effect glucocorticoids carry out in a liver effect anabolic, namely proteins — enzymes, specifically responsible for neoglucogenesis, transamination, and also synthesis of albumine of a blood plasma activate synthesis of system. At the same time for synthesis of protein in a liver the amino acids released at destruction of structures of other bodies and a lot of available in blood are used. Such effect of redistribution of structural resources in the form of amino acids, and it is possible, nucleotides and other connections makes biol, the maintenance of a syndrome stress (see) as nonspecific component of adaptation in general and compensations in particular.

So, it is known that at the first considerable physical. loadings at people and animals the syndrome of a stress develops: concentration of glucocorticoids in blood increases, there is an eosinopenia, an atrophy of a thymus gland, reduction of body weight. It turned out further that this classical catabolic effect is naturally combined with activation of synthesis nucleinic to - t and proteins in a myocardium and skeletal muscles.

Creation in the operational way of a considerable stenosis of the mouth of an aorta at animals is followed by development of a stress; at the same time in a myocardium develop compensatory hyperfunction and then a hypertrophy. Such damages as removal of one kidney, hepatic lobes, a lung etc., naturally are followed by development of a stress and catabolic effect of glucocorticoids in many fabrics and bodies; however against the background of this generalized catabolic effect activation of synthesis nucleinic to - t and proteins in the remained bodies quickly develops and they quickly hypertrophy.

Thus, at a stress there is a transfer of resources from the systems which are not participating in adaptation to this specific factor in the systems specifically responsible for this adaptation, and in particular for compensation.

As a result of such redistribution oxygen, substrates of oxidation, and also the predecessors used for synthesis nucleinic to - t and proteins, directionally come to the systems which are carrying out compensatory hyperfunction i.e. to systems where the structural trace which makes further a basis of long-term compensation forms.

The role of a stress at a stage of urgent compensation and in the course of its transformation into compensation long-term consists that this the nonspecific, implemented at the most various damages component of compensation exponentiates formation of the system structural trace making a basis of long-term specific compensation specific funkts, the defect caused by this damage. General mechanism K. the item is submitted on the scheme 2.

Scheme 2. General mechanism of compensatory process. The mechanism of compensatory process can be presented as follows: the disturbing factor breaks a homeostasis. These disturbances through the highest regulatory centers activate systems of specific and nonspecific compensation. The created system of specific compensation carries out the compensatory hyperfunction which is followed by mobilization funkts, a reserve and deficit of energy in cells; the system of nonspecific compensation realizes a syndrome of a stress. The urgent, but unreliable compensation which arose thus to some extent limits funkts, defect and the related disturbances of a homeostasis. At the same time in cells of system of specific compensation the interrelation between function and the genetic device is implemented — activation of synthesis nucleinic to - t and proteins develops; thanks to a syndrome of a stress the increased flow of oxygen, substrates of oxidation, and also predecessors nucleinic to - t and proteins goes to cells of this system. In a result in compensating funkts, system the structural trace eliminating deficit of energy in cells of system and increasing its power and funkts, a reserve forms. It provides elimination or reduction funkts, the defect caused by damage and disturbance of a homeostasis — rather steady long-term compensation is established.

The main stages of compensatory processes

Compensation, as well as any other long-term adaptation reaction, can take place four main stages.

1. The stage of urgent compensation is characterized by compensatory hyperfunction specific compensating funkts, systems and the expressed syndrome of a stress. In case other adaptive reactions of the damaged organism quickly liquidate funkts, defect, To. items are limited to this stage. So, at blood loss recovery of quantity of erythrocytes by direct regeneration stops To. item. At experimental To. the item inhibition of synthesis of RNA on structural genes of DNA by means of Actinomycinum breaks implementation of interrelation between function and the genetic device and interferes with development of a system structural trace and artificially limits To. item stage of urgent compensation. In these conditions compensatory hyperfunction of heart, kidney, a hepatic lobe does not lead to a hypertrophy of these bodies; animals perish at the phenomena of a heart, renal, liver failure.

2. The transition phase from urgent compensation to long-term is characterized by a combination of compensatory hyperfunction and a syndrome of a stress to activation of synthesis nucleinic to - t and proteins in cells specific compensating funkts, systems and development of a system structural trace. In process of development of this stage funkts, the defect caused by damage, a syndrome of a stress, deficit of energy in cells of the compensating system gradually are liquidated.

3. The stage of steady long-term compensation is characterized by elimination or considerable reduction funkts, defect, existence of the created structural trace in compensating funkts, system and minimum activation of synthesis of protein in cells of this system, edge is necessary for updating of the increased mass of structures. Duration of this stage at heart diseases, loss of one kidney or lung in many cases can correspond to specific life expectancy.

4. The stage funkts, insufficiency can develop at big initial funkts. defect and excessive hyperfunction and a hypertrophy of the compensating systems, and also as a result of additional damages of an organism.

In a habit view compensatory hyperfunction of this stage differs from evolutionarily provided increase in functions which is periodically arising in a healthy organism (such increase in function is always temporary and is replaced by the period of relative rest). Compensatory hyperfunction of the escaped nerve centers, the only kidney or heart at damage of the valve device, on the contrary, is continuous because owing to irreversibility of the damages which arose in an organism the continuity of hyperfunction is vital need.

The stage funkts, insufficiency marks transition To. the item in decompensation (see) also can develop at the expense of two main mechanisms. The first of them consists that at a big hypertrophy growth of cells is unbalanced and is followed by selective lag of mass of the structures responsible for ionic transport, power supply and use of energy for implementation fiziol, functions. Such situation is studied in depth for the expressed compensatory hypertrophy of heart. The second mechanism consists that after the long period of hyperfunction and a hypertrophy in a nervous system, closed glands and executive bodies the peculiar complex of local wear which is expressed in decrease in synthesis nucleinic to - t and proteins, disturbance of updating of structures, death of a part of cells and development of an organ sclerosis can develop.

Formation To. the item at any damage of an organism in many respects depends on its previous state and can be stimulated various factors. Existence at the person of diverse movement skills and their development in the course of the prof. of training or to lay down. physical cultures promotes compensation at damages of a nervous system and musculoskeletal system. At the people trained to physical. to loadings, compensation of heart diseases proceeds more absolutely. Positive influence on development To. the item, and first of all on transition of urgent compensation to steady long-term, renders good nutrition.

Compensatory processes at damage of a nervous system

Compensatory processes at damage of a nervous system are most perfect. So, during removal of one cerebral hemisphere or a cerebellum at dogs after the period funkts, frustration compensatory activity of the remained departments of a brain provides normalization of the movement. At the person inborn lack of a cerebellum can be also compensated by activity of other parts of the nervous system. At back disturbance of functions of a motor analyzer is compensated to tabes by activity of the visual analyzer. An important role in development To. items at damage of a nervous system play two factors.

1. Multilinearity and a versatility of anatomic bonds between various parts of the nervous system. At destruction of one of ways of communication function of the destroyed way is undertaken by other nervous cells. This feature of a nervous system creating ample opportunities for compensation of its damages, I. P. Pavlov called mechanical immunity.

2. The plasticity of nerve centers which is expressed that under the influence of the afferent alarm system, new on the structure, arriving from the periphery after damage there is as if a reeducation of neurocytes: they change speed and a rhythm of the activity. As a result also the efferent alarm system changes thanks to what nerve centers can assume in the course of compensation new, not inherent to them before function (see. Plasticity of physiological functions ). So, e.g., the center of a vagus nerve can assume function of the center providing an innervation of an extremity, the centers of flexor muscles can carry out function of the centers of razgibatel. These data confirm a crucial role of an afferent impulsation in formation compensating funkts, systems at injury of a brain.

Most plasticity is inherent in a cerebral cortex, edges plays a crucial role in compensation at considerable damages of a nervous system. Researches E. A. Asratyana (1938 — 1956) with sotr. allowed to establish that the cerebral cortex plays the leading role in compensation of the motive disturbances arising at half section of a spinal cord, a deafferentation and removal of extremities, a cerebellum and vestibular mechanism, section of nerves. If at the same time to dogs to remove a cerebral cortex, dysfunctions of the movement are never compensated; at animals with the kept bark, on the contrary, gradual development of compensation is observed.

A role of a cerebral cortex in To. the item at injury of underlying parts of the nervous system is defined by the fact that cortical analyzers sensitively react to any change of relationship of an organism with the environment. After the thin analysis of new afferentation which begin to come to bark after damage in it on the basis of uslovnoreflektorny synthesis the functional combinational centers providing more intensive form new, according to I. P. Pavlov, and also qualitatively new use of the efferent devices which escaped at damage is frequent.

E. A. Asratyan allocates three types of influence of bark promoting compensatory reorganization of underlying departments of c. N of page 1. The descending influence of bark defining excitability, lability, a tone and operability of the subcrustal centers. 2. The Bezuslovnoreflektorny activity of bark providing perfection of implementation instinctive reflexes (see).

3. Uslovnoreflektorny activity of bark, its ability to form new conditioned reflexes (see) by means of which the most perfect compensation is reached.

The crucial role of cortical activity in compensation of disturbances of the movement after wounds and recovery operations at the person is explained by it. E.g., after operation of splitting of a forearm (creation of a hand of Krukenberg) there are only anatomic premises for compensation of the absent brush. In order that AGAIN formed «branches» of a hand to some extent assumed function of the absent brush, the profound changes of functions of a shoulder and forearm caused by reorganization of the corresponding nerve centers are necessary. Without training based on a verbal explanation and display of elementary labor skills, such reorganization is impossible even for a number of years. Vigorous activity of cortical mechanisms, in particular mechanisms of the second alarm system in this case is necessary for development of compensation.

Extent of participation of a cerebral cortex in compensation of various damages of a nervous system at animals is not identical. E.g., compensation of damages at section x / 4 a spinal cord can happen at the animals deprived of a cerebral cortex. At young animals compensation proceeds with smaller extent of participation of cortical mechanisms. The highest parts of the nervous system, taking part in development To. items, are capable to compensate by the activity of dysfunction of the movement,

S. I which are shown in the form of a flexion contracture and caused by existence in the relevant centers of a spinal cord of the phenomena of congestive excitement». Frankstein (1948) established that if to make decerebration at externally healthy animal, at to-rogo in the past there was on one of extremities an inflammatory process and a protective flexion contracture, then against the background of the general cerebrate rigidity to dominance of a tone of razgibatel there is a recovery of the existing earlier flexion contracture of one of extremities. The similar phenomenon was observed at people after administration of the novocaine breaking the alarm system from the periphery and the defiant phenomenon of braking in cells of bark; at the same time temporary recovery of the existing earlier spastic paresis, the painful centers, stutters etc. was noted. In this regard it is possible to conclude that disappearance patol, the phenomena was caused by influence of the highest parts of the nervous system, a cut compensated the inert center of excitement which developed in subcrustal area and a spinal cord.

At development To. the item the compensating mechanism which is most made for this situation quite often forces out less perfect. By I. Pavlov it was shown that during full removal of a cerebral cortex at animals recovery of the movement happens several times quicker, than during removal only of a front half of bark. Such phenomenon is explained by the fact that residual function of the remained sites of bark as if serves as the hindrance interfering the introduction of the most perfect for given patol, situations of the compensatory mechanism — motoriums of subcrustal educations; full removal of bark involves dominance of subcrustal educations and implementation of all compensatory opportunities.

I. P. Pavlov's data were confirmed with experiments of Trendelenburga (W. Trendelenburg, 1915), Oden and Franz (Oden, Franz, 1917) who showed that after removal of both motor zones of bark at animals compensation of motive disturbances happens quicker, than after a unilateral extirpation of a motor zone. In these experiments dominance of the basic which is most made for these conditions of the compensating mechanism was reached in the surgical way. Dominance of the main compensating mechanism and the most perfect compensation are reached by means of natural braking of the minor, less perfect compensating mechanisms. So, e.g., at the patients having motor aphasia the remains of speech function in the form of so-called residual set phrases usually remain. It is noted that at recovery of the speech in the course of training or spontaneously there is a disappearance of residual set phrases. At the same time set phrases disappear slightly earlier, than there are signs of recovery of the speech that sometimes it is incorrectly perceived as an aggravation of symptoms of the patient.

The phenomena of mutual replacement of the compensating mechanisms receive the most convincing explanation in the light of the doctrine about to a dominant (see), developed by A. A. Ukhtomsky, also give the grounds for the conclusion that the reflex mechanism playing the main role in compensation becomes the mechanism dominating in regulation of the broken function; it provides braking of less effective compensatory mechanisms and the most perfect for these conditions of development To. the item

the Compensatory hypertrophy of heart

the Compensatory hypertrophy of heart is the main factor of compensation at diseases of bodies of blood circulation. This phenomenon is provided with increase in synthesis nucleinic to - t in cells of a myocardium that leads to increase in weight, i.e. to a true hypertrophy of myocytes, a hyperplasia of fibroblasts and other connective tissue cells of a myocardium; the hyperplasia of muscle cells, on a nek-eye to data, can be observed at significant increase in mass of heart, a result is increase in mass of heart by 1,5 — 2,5 times.

On an etiology distinguish two options of a compensatory hypertrophy of heart at disturbances of blood circulation: the hypertrophy which arose owing to a long overload of heart i.e. a hypertrophy of heart from hyperfunction, and the hypertrophy of heart which resulted from direct injury of a myocardium; there is an option when these factors are combined.

The compensatory hypertrophy of heart from hyperfunction develops at heart diseases, a hypertension, arteriovenous shunts, hypertensia of a small circle of blood circulation, in connection with increase in tension of a myocardium in a systole. This phenomenon leads to the fact that the increased consumption of ATP in myofibrils advances its resynthesis in mitochondrions. Concentration of ATP and creatine phosphate decreases at simultaneous increase in concentration of products of their disintegration, and as a result the size Russian Federation increases. This shift implicates: first, process of resynthesis of ATP in mitochondrions is activated via the mechanism of interface of oxidation to phosphorylation, i.e. power ensuring urgent compensation of heart at loading is created; secondly, the increased size Russian Federation leads to formation in cells of a myocardium of a signal which activates synthesis nucleinic to - t and by that turns on the main mechanism of long-term compensation — a hypertrophy hearts (see).

Biol, value of a hypertrophy of heart at an overload consists that at the same time distribution of the increased function of heart in its increased weight is provided, systolic tension decreases and the size Russian Federation is returned to initial level. Such decrease in originally increased tension of a myocardium to norm is proved at people with heart diseases and a hypertension now. It means that the hypertrophy compensates excessively big load of heart by decrease to norm of function of a myocardium.

The compensatory hypertrophy of heart develops at coronary heart disease, myocardites, hereditary cardiomyopathies. These diseases are characterized by the fact that load of heart can be and not increased, but nevertheless there is a deficit of vysokoergichesky connections and, therefore, the size Russian Federation increases. It occurs because at a lack of oxygen, dissociation of oxidation and phosphorylation, hereditary defects of mitochondrions and myofibrils synthesis of ATP becomes insufficient for maintenance of normal function. Owing to increase of the size Russian Federation there is a signal activating synthesis of nucleic acids and protein; the hypertrophy of heart develops. This form of a hypertrophy is proved patomorfol. and echocardiographic researches at coronary heart disease and method of a two-plane film X-ray analysis at a cardiomyopathy. It is essential that at these diseases the hypertrophy of heart develops without any additional load of heart and precedes disturbances of sokratitelny function. Biol, value of a hypertrophy of heart is defined by the fact that originally it arises against the background of normal function, and further leads to decrease in systolic tension of ventricles of heart to abnormally low level. At the same time thanks to increase in mass of heart in general systolic pressure in its ventricles, shock and minute volumes long remain normal — the hypertrophy of a myocardium compensates inferiority of the injured myocardium due to increase in weight.

Both options of a hypertrophy of heart, despite a different etiology, develop on the basis of the same mechanism and for a long time prevent insufficiency of heart. The mechanism and compensatory value of the main options of a hypertrophy of heart are shown on the scheme 3.

Scheme 3. Mechanism of a compensatory hypertrophy of heart. The mechanism of a compensatory hypertrophy of heart can be presented as follows: at the diseases increasing load of heart — defects, an idiopathic hypertensia, arteriovenous shunts — the systolic tension of a myocardium and a consumption of ATP in myofibrils ah increases. At the diseases causing direct injuries of a myocardium — an ischemic disease, myocardites, hereditary cardiomyopathies — there is a decrease in resynthesis and efficiency of use of ATP. As a result both groups of diseases lead to nek-rum to decrease in concentration of vysokoergichesky connections (ATP and creatine phosphate) in a cardiac muscle, and this shift indirectly through a factor regulator activates the genetic device of myocytes — increases in them intensity of synthesis nucleinic to - t and proteins, the compensatory hypertrophy as a result develops, edges increases the mass of heart and by that reduces the systolic tension and a consumption of ATP per unit mass of a myocardium. As a result deficit of ATP in a myocardium decreases, insufficiency of heart does not develop. The hypertrophy is stabilized at the certain level, reduces the systolic tension (it is shown by a dotted line) that provides rather steady compensation.

It is long the compensatory hypertrophy existing and progressing owing to the accruing loading or damage insufficiency of hypertrophied heart can gradually be transformed in hron; this phenomenon represents one of many examples of transition of adaptive reaction to pathological. Transition of a compensatory hypertrophy in heart failure (see) is important in clinic; development of insufficiency is defined to a large extent by the fact that increase in mass of body at the expressed hypertrophy develops as an unbalanced growth form.

This disharmonic growth at the level of body is expressed by ratio distortion between the mass of heart and its adrenergic nervous device — growth of the neurocytes and their axons regulating function of heart lags behind increase in mass of heart, resynthesis of noradrenaline lags behind its expense. As a result density of an arrangement of sympathetic fibers and concentration of a mediator in a myocardium decrease several times. At the same time the adrenoreaktivnost of heart decreases that, apparently, is caused by decrease of the activity of adenyl cyclase. Regulation of cordial activity is as a result broken.

Disharmonic growth is shown in lag of increase in quantity of capillaries of heart from increase in quantity of myocytes. As a result of it the quantity of capillaries per unit mass of a myocardium decreases, the diffusion distance for oxygen increases. At loading it leads to a hypoxia in hypertrophied muscle cells and to limitation of resynthesis of ATP in mitochondrions.

In a muscle cell results of disharmonic, disproportionate growth are especially expressed. The volume of a muscle cell increases in much bigger measure, than its surface; so, the area of a sarcolemma, in a cut the most important mechanisms of ionic transport are localized, counting on a mass unit of a cell decreases by 2,5 times. As a result the power of Na-K-and the Na-Ca-pump, by means of to-rogo is removed Ca from a sarcoplasm on extracellular Wednesday, also the power of the calcic pump of a sarcoplasmic reticulum decreases, decreases. It leads to the slowed-down removal of calcium from a sarcoplasm, according to the slowed-down relaxation of a myocardium and development of a syndrome of an imperfect diastole. Its increased receipt in a mitochondrion is a consequence of incomplete removal of calcium from a sarcoplasm that reduces an exit of ATP and reduces efficiency of oxygen consumption by a cardiac muscle.

In molecular structures disharmonic growth can lead to the fact that the quantity of long-living light chains in heads of a myosin increases to a large extent, than quantity of short-lived heavy chains. As a result decreases ATF-aznaya activity of myofibrils and their ability to use energy of ATP.

Thus, compensatory, the hypertrophy of heart prevents an acute heart failure and at the same time is followed by decrease in effective adrenergic regulation, ionic transport, power supply and reduction of ability of myofibrils to transform chemical energy of ATP to mechanical energy of muscular contraction. It in turn leads to the fact that the maximum speed, amplitude and force of reductions of hypertrophied heart are reduced, the maximum number of work is also reduced, a cut the mass unit of a hypertrophied myocardium can generate. This complex of changes is proved for the expressed compensatory hypertrophy which is usually developing at disturbances of blood circulation; the moderate hypertrophy of heart which is naturally developing as a result of trainings and physical. loadings, it is characterized by opposite structural changes and increase funkts, opportunities of a myocardium (see. Heart ). At the expressed hypertrophy of heart decrease funkts, opportunities of a myocardium makes a basis of the insufficiency of hypertrophied heart developing further. This idea of the mechanism of insufficiency of hypertrophied heart is represented on the scheme 4.

Scheme 4. Pathogeny of insufficiency of hypertrophied heart. The pathogeny of insufficiency of hypertrophied heart can be presented as follows: the considerable compensatory hypertrophy preventing insufficiency of heart at basic diseases of blood circulation leads at the same time to deceleration of power of system of adrenergic regulation, ionic transport, power supply of a cardiac muscle and reduction of ability of myofibrils to use energy of ATP. These shifts are interconnected and in total reduce force and speed of reduction of a myocardium. As a result the preinsufficiency of heart which is characterized by incomplete exile of blood from a cavity of ventricles, increase in diastolic pressure, initial decrease in minute volume develops. Shifts of a hemodynamics, depending on the expressiveness and a condition of an organism, can activate a chain of the phenomena. First, the factors of compensation providing unloading of heart and constraining transition of preinsufficiency of heart to heart failure are activated noncardiac. Such factors are activation of an erythrocytopoiesis, increase in power of system of mitochondrions in fabrics and ability of fabrics to absorb oxygen from blood, and also the decrease in a physical activity of an organism and standard metabolism regulyatorno caused. Secondly, the renin-angiotenzinnaya system can be activated, edges promotes loss of potassium, a delay of sodium and water, development of hypostases and ascites, and as a result — to transition of preinsufficiency to insufficiency of heart. On the scheme the chain with a minus sign (—) designates noncardiac shifts which prevent heart failure; with a plus (+) designate the shifts exponentiating development of heart failure.

Insufficiency of heart develops not right after possibilities of a myocardium decrease funkts. This phenomenon for many years can be prevented at the expense of two major factors. First, defect of sokratitelny function of a hypertrophied myocardium is for many years blocked by increase in its weight. Secondly, initial shifts of a hemodynamics through neuroendocrinal regulation brake standard metabolism and a physical activity of an organism; on the other hand, noncardiac factors of compensation — an erythrocytopoiesis, ability of fabrics to absorb oxygen from hypoxemic blood etc. are activated. This chain of the phenomena slows down developing of heart failure. It promotes preservation of brittle balance, a cut is designated as «preinsufficiency of heart».

At a further course of a disease the progressing decrease in sokratitelny function of heart leads to such increase in venous pressure and decrease in minute volume of heart which cause intensive excitement a renin-angiotenzinnoy of system (see. Angiotenzin ), at the same time there is a loss of potassium and a delay of sodium and water in an organism. This shift in combination with a hydraulic factor not only plays a direct role in development of hypostases and ascites, but causes additional suppression of sokratitelny function of heart since cells of a myocardium are deeply damaged at deficit of potassium; this chain leads to development of heart failure.

The condition of the patient at each stage of a disease (existence of so-called preinsufficiency or insufficiency) is defined by extent of changes in a myocardium and a ratio of the regulatory reactions which arose in response to changes of a hemodynamics. The changes of action of the heart and a hemodynamics developing at heart failure of various etiology are characterized by a certain community. At the same time the wedge, a picture of heart failure, napr, at a myocardial infarction, heart diseases, etc., has the characteristic features.

Therapy of heart failure in essence represents a complex of the influences regulating a dynamic equilibrium of factors of damage and factors of compensation. In each case it is defined by an opportunity operational or pharmakol, impacts on an overload and damage. Reversibility of processes of a hypertrophy of a myocardium of heart of the person in principle is proved; therefore, the negative shifts caused by a hypertrophy to some extent are reversible.

Change of compensatory processes in advanced and senile age

According to the adaptation and regulatory theory offered by V. V. Frolkis (1970) during the aging happens not only fading of exchange and function, but also emergence of important adaptive mechanisms (see. Old age, aging ). At the same time the general result of these changes consists in easing of intensity To. item. Easing To. the item limits ability of the elderly person to adapt to changes of the environment; vulnerability of an organism increases, patol, processes develop easier.

Even at not changed vital indicators (level of sugar in blood, osmotic, oncotic, intraocular, arterial pressure) reliability of regulation homeostasis (see) decreases, and it leads to the fact that changes of exchange and function at elderly people, even at small loadings, can gain long character, i.e. the initial level of life activity of an organism is recovered more slowly. So, it is shown that during the performance of various muscular exercises the possible amplitude of change of the ABP, cordial emission, cardiac performance, vital capacity of lungs, than lung ventilation at men of 60 — 70 years is less, than at 20 — 30-year-old. Duration of the recovery period at elderly people increases by 1,5 — 2,5 times, and after achievement of initial level of blood circulation and breath quite often again there are disturbances of these functions. At sugar loadings, especially double, at 60 — 70-year-old people more high level of sugar in blood and its slowed-down recovery in comparison with 20 — 30-year-old people is noted.

Decrease To. to the item in old age it is established at the different levels; it defines the most important mechanisms of aging. Potentialitys of the genetic device of cells are limited, activation of biosynthesis of protein in this connection such compensatory reactions as a hypertrophy of cells and bodies during the strengthening of function of body are less expressed is slowed down. There can be an oppression of activity of the genetic device in conditions which cause optimum reaction in juveniles. So, at daily introduction to old rats of a hydrocortisone in a liver for the tenth day suppression of synthesis of a number of enzymes, is noted by information and ribosomalny RNA, and young adult rats have an activation of the same processes. Decrease in mitotic ability of cells — one of the main reasons for aging — weakens processes of regeneration. Shifts in compensation at different stages of process of generation of energy in a cell, the oxygen mode in an organism are important: range of possible increase in lung ventilation, oxygen consumption, strengthening of blood supply of fabrics, strengthenings of tissue respiration, growth of activity of respiratory enzymes, updating of makroertichesky connections, etc. is reduced.

The extreme importance in restriction To. items have shifts in neurohumoral regulation, century of N of. At elderly people conditioned reflexes are more slowly developed, processes of braking are weakened.

Changes of the basic nervous processes limit the most dynamic mechanisms of adaptation of an organism to the environment, reduce working capacity. The general adaptation syndrome has less expressed compensatory value. In old age at repeated irritations disturbance of functions of gipotalamo-pituitary system develops quicker, there comes the stage of exhaustion quicker.

Compensatory mechanisms change in old age not only quantitatively, but also is qualitative: smaller amounts of many hormones, mediators, metabolites cause changes of exchange and function; many To. items join more slowly; have the reduced amplitude, long character; arise more often and serious violations of exchange and function are more sharply shown. Weakening of nervous influences leads to essential change of a trophicity of fabrics.

The adaptive mechanisms arising in parallel with it in many respects define life expectancy. These processes consist in increase in number of kernels in many cells in the conditions of decrease of the activity of the genetic device, growth of intensity of glycolysis against the background of weakening of tissue respiration, sensitization of fabrics to a number of hormones (thyroxine, adrenaline, insulin) at depression of function of hemadens, etc. However such compensatory and adaptive mechanisms not can is long to maintain stable state of an organism; gradually ability of an organism to adapt to changes of the environment everything decreases.

The irritants causing optimum reaction in a young organism in old age can lead to gross violations of exchange and function. So, strong pain stimulation at mature animals leads to increase in the ABP, cordial emission, lung ventilation, at old animals — to sharp oppression of a hemodynamics and breath, at them shock easily develops. In old age the hypoxia develops, and it promotes development of coronary heart disease, disturbance of cerebral circulation, etc. Leads weakening of nervous control and change of reactions of fabrics to humoral factors to developing of pathology (hormones, metabolites, etc.).

Structural bases of adaptation, compensatory processes

Development morfol, aspects of a problem of adaptation of an organism to environmental factors and compensation of the functions broken at various patol, processes was limited generally fabric and organ to levels until recently. Such questions as the general dynamics and morfol, bases of an inflammation, fabric regeneration, processes of the organization, adaptive reorganization of various bodies and some other, received rather detailed and versatile lighting. However thinner, intracellular structural changes, to-rymi are followed adaptive and compensatory reactions of an organism, long time remained out of sight of morphologists owing to limited methodical opportunities. The light microscope allowed to observe only relatively rough, rather slowly developing and also slowly taking place structural changes, without giving the chance to catch a material basis of continuous adaptive fluctuations of functional activity of the cells and fabrics which enough are accurately registered by means of physiological, biochemical and other methods. As a result of lag morfol, the analysis of processes of compensation and adaptation from physiological in 19 century and in the first third of 20 century the problem of adaptation of an organism to conditions of the environment was lit unilaterally, is preferential from functional positions. On this soil there were well-known ideas of bigger lability of function, than structures, that functional changes arise before morphological and unlike the last are easily reversible and that in many not hard cases these «purely functional» changes and limit reactions of an organism to external influences.

This view of a ratio of functional and structural changes was changed in connection with development submicroscopy (see), histochemistry (see), autoradiography (see) and other methods of a research which allowed to study morphology of intracellular processes. During these researches ideas that in biol, systems there can be «purely functional» changes which are not followed structural yet dissipated. The doctrine about adaptation, adaptive and compensatory processes became essential to change, being more and more filled morfol, contents and losing the in the past unilateral functional character. Use of new opportunities of the structural analysis biol, processes allowed to lay the foundation of ideas of the most general principles of material security of adaptive and compensatory processes and their private manifestations in this or that body.

The most common feature of all various adaptation and compensatory reactions of an organism consists in what at the heart of an equilibration of an organism with the environment both in normal conditions of life activity, and at various diseases lies, finally, always same biol a phenomenon — continuous change of intensity of biosynthesis according to the changing living conditions. Electronic avtoradiografi-cheskiye researches demonstrate that intensity of biosynthetic processes is not identical not only in different cells and in the organellas of each cell of the same name, napr, in its mitochondrions, kernels, etc., but even within one organella. It means that at each this moment from total number of the structures of the same name only their some part while others stay in a condition of relative functional rest intensively functions.

At adaptive strengthening of functional activity of body the number of cells, and also the ultrastructures in each cell differing in intensive biosynthesis as appropriate increases. This process covers both nuclear, and cytoplasmatic structures. An example of adaptive fluctuations of functional activity of the nuclear device is relationship eu-and heterochromatin. Heterochromatin represents condensed, nesintezir an uyushcha yu, the «based» part of nuclear chromatin (see) while euchromatin — its active part, on matrixes of DNA the cut is intensively synthesized by RNA. Therefore, increase in volume of euchromatin and the reduction of volume of heterochromatin corresponding to it (total quantity of chromatin in a cell is stable) speaks about strengthening of function of a cell; opposite changes demonstrate its transition to a condition of relative rest. By means of an electronic and microscopic autoradiography it is possible to monitor interconversions eu-and heterochromatin, i.e. to investigate process of activation or snubbing of function of the main regulatory device of a cell. The given example concerns structurally functional relationship within one organella, in this case a kernel. Essentially the same process of gradual involvement of the increasing number of structures in active work of a measure of increase of a functional load is traced also at other levels of the organization, namely in relationship between the organellas of the same name, cells, segments and shares of body.

Results of electronic and autoradio graphic researches do not leave doubts that to a certain level of functional activity of body at each this moment there corresponds the number strictly certain, equivalent to it of intensively synthesizing (renewed) cells and intracellular structures. The biopower sense of asynchrony of running cycles of the structures of the same name consists most likely that thanks to it for each structure uniform alternation of the periods of functional activity and rest, i.e. optimal conditions for its phisiological regeneration is provided. Thus, the first principle of material security of adaptation fluctuations of functional activity of bodies is that these fluctuations are provided on the basis of change of number of actively working structures from among available.

But the functional load on system, napr, on a cell, can increase or be long, and then for preservation of a homeostasis only of one inclusion in work of the available ultrastructures it is already not enough because the volume of function demanded from a cell exceeds that limit, to-rogo it can reach under a condition even of simultaneous work of all its organellas. Not less important and another: even if the number of the available ultrastructures is formal and it is possible to consider sufficient, then not alternate, but synchronous work of the majority them or even everything, breaking the principle of the alternating functional activity and by that a normal current fiziol, regenerations, already in itself shall be followed by the progressing deficit of structures, development of dystrophy, and then and a necrosis of a cell. That and in these, chronically intense, working conditions to keep the principle of alternate inclusion of ultrastructures in active function, i.e. to support such level of their regeneration, to-ry would provide an equilibration of intensively current processes of disintegration with so intensive processes of synthesis, in a cell the number of ultrastructures, and also the sizes of each of them increases, i.e. occurs hyperplasia (see) and hypertrophy (see).

The hyperplasia of cytoplasmatic structures, actionees of specific function of this cell, is followed by the corresponding hyperplastic processes and the nuclear device: the sizes and number of the kernels responsible for synthesis of RNA increase, there is a poliiloidization of a kernel, i.e. increase in amount of DNA, a kernel hypertrophies or two-nuclear cells are formed. Such hyperplastic processes are developed in muscle cells strenuously of the working myocardium, in fibroblasts of granulyatsionny fabric, in hepatocytes, a renal epithelium at a compensatory hypertrophy of a kidney and in cells of other bodies. As a result of these nuclear cyto-plasmatic changes «material resources» of a cell extend and it can even carry out intense activity according to the principle of the alternating activity of structures, i.e. at preservation of balance between dissimilation and assimilation. This adaptive reaction revealed by means of a light microscope is expressed in a hypertrophy of a cell — the known phenomenon which received modern structural interpretation. Similarly, i.e. like increase in number of ultrastructures of a cell, at a long intensive functional load there is also an increase in number (hyperplasia) in cells of bodies. Thus, the second principle of material security of an adaptation intensification of functions consists in increase in number of structures (organellas of cells and cells) according to the functional tension demanded from body. This mechanism is especially characteristic of cases when the organism a long time is in a condition of the increased functional activity or when it needs to fill the defect of fabric which resulted patol, process.

Very important condition of adequate structural ensuring adaptation fluctuations of activity biol. processes temporary synchronization between the action of an irritant demanding change of functional activity of body and the moment of implementation of the last is. If the ratio between force of external influence and number of actively functioning structures can be considered as the quantitative party morfol, characteristics of reactions of adaptation and adaptation, then rate of mobilization of material resources represents their major qualitative criterion: the material resources of body quite sufficient potentially, but not realized in time, i.e. synchronously with action of a pathogenic factor, cannot prevent it destructive influence.

Studying of features of compensatory and adaptive reactions of an organism in continuously changing conditions of the environment shows that one of the most important properties of these reactions is lability of a rhythm fiziol, regenerations of structures (organellas of cells), i.e. ability of an organism to change intensity of their expenditure and new growth depending on frequency and force of action of various factors of surrounding and internal environment and by that to level ratios between speeds of these two opposite p rotsess. In this mobility of regenerator processes one of the most important mechanisms of bystry and adequate adaptation of an organism to the changing working conditions is put as is normal, and at various patol, states. In morfol, the relation the essence of this adaptive reorganization biol, rhythms consists that at various changes of frequency of action of an irritant intensity of phisiological and reparative regeneration every time is established at the level preventing deficit of structures incompatible with life. Thus, the third principle of material security of adaptation strengthening of functions consists that at the same time there is not a simple increase in number of actively functioning structures, and it, intensity to-rogo continuously fluctuates in strict accordance with changes of frequency and force of action of an irritant. Emphasizing high lability of a rhythm of updating of intracellular structures, its ability to be reconstructed quickly according to the changing frequency and force of external influences, it is necessary at the same time to note that this ability of an organism to reorganization of intensity biol, processes is not boundless: there are nek-ry minimum terms of expansion of this reorganization, earlier to-rykh it under no circumstances cannot occur. So, e.g., autoradio graphic researches show that DNA replication, i.e. emergence of its new matrixes, happens not earlier than in 24 — 30 hours after the beginning of action of a pathogenic factor and that how the dose of the last or frequency of its influence increased, this term will remain invariable. DNA replication provides either emergence of new cells, or a hypertrophy of existing. Until it occurs, the cell uses those resources, to-rye at it are available by the time of action of an irritant, and it is expressed, in particular, in an intensification of synthesis of RNA: it is developed due to inclusion of the structures which before were not participating in synthesis and there is it immediately, practically along with the beginning of action of an irritant. On value for preservation of life of the damaged cell such strengthening of synthesis of RNA can be considered as an emergency measure, and strengthening of synthesis of DNA — as radical, long-term. Thus, representations of biochemists about «immediate», «urgent» and stronger and powerful «chronic» forms of adaptation of exchange are confirmed also at the ultrastructural level. In respect of a problem of structural bases of adaptation these data are of interest in the respect that they once again emphasize the main thesis: whatever was the form of adaptation in each case, be it even the most urgent, almost immediate adaptation, it is never carried out on «purely functional» to a basis, always having under itself the corresponding material resources. This base is continuous regeneration of structures of an organism and their hyperplasia. At the same time intracellular regenerator and hyperplastic processes have special value (see. Regeneration ). This results from the fact that any function of an organism, eventually, is derivative of processes of disintegration and synthesis of the substances flowing at molecular level i.e. from intracellular updating. As for updating of number of cells and their hyperplasia, they provide adaptive fluctuations of functional activity not directly, and indirectly, by change and increase in number of large working blocks (cells), inside to-rykh and processes are developed corresponding biochemical. If at the same time to consider that in nek-ry bodies (a myocardium, c. N of page) cellular updating or is very poorly expressed or at all is absent, that value of intracellular regeneration as structural basis of processes of adaptation acts even more clearly. Thus, it is possible to speak about the uniform principle of structural ensuring adaptive and compensatory processes, to-ry consists in recovery (regeneration) of ultrastructures and their new growth (hyperplasia).

The wedge, aspect of relationship of structural and functional changes in process of adaptation of an organism to action of pathogenic factors is especially important. It first of all concerns so-called dystrophic changes of internals. There is a representation that these changes are characterized by disturbances of colloidal composition of a kernel and cytoplasm and are limited generally biochemical, level. Quite so, in particular, G. F. Lang understood essence of the concept entered by it and widely adopted about dystrophy of a myocardium, or myocardial dystrophies (see). Numerous electronic microscopic examinations demonstrate that idea of a myocardial dystrophy as about disbolism, primary in relation to morfol, to changes of cardiomyocytes or as about process, at Krom «morphological changes in a myocardium are not found or when they do not correspond to character and extent of functional disturbances», is outdated. A wedge, to manifestations of a myocardial dystrophy at all stages of its development there correspond accurate structural changes of the miofibril-lyariy device of muscle cells, their mitochondrions, a sarcoplasmic reticulum, intranuclear organellas, etc. At the same time functional changes not only do not hold the advancing position in relation to structural, but, on the contrary, a wedge, symptoms of a myocardial dystrophy, as well as dystrophic changes of all other bodies, appear, as a rule, after emergence of ultrastructural changes of their cells. It is explained by the fact that pathogenic factors cause first of all damage of various membrane structures of a cell. Practically in parallel with it there comes the intensification of the intracellular regenerator and hyperplastic processes providing a bystry new growth of ultrastructures of a cell and by that preservation of necessary level of its functional activity. Autoradio graphic researches demonstrate that even the expressed changes in one part of a cell can is long to be compensated by regenerator processes in other its part and essentially not to affect function. The last is broken only when structural intracellular changes reach very high degree and more cannot be leveled by regenerator and hyperplastic processes any more. Therefore, morphologically changed cell can be functionally normal. In the same way and at the level of body and system extent of functional disturbances at this or that patol, process is defined by a mutual ratio of destructive and regenerator processes and therefore in the presence of the progressing structural changes neutralized by active regenerator reaction, the person quite often can remain a long time almost healthy, i.e. adapted to the environment. And only when morfol, changes reach considerable degree and cannot be completely compensated, the first wedge, symptoms of a disease appear. Told the wedge, symptoms of this or that disease at far come stages of its development, quite often already incurable is confirmed by numerous cases of emergence of the first (malignant tumors, cirrhosis, calculous cholecystitis, coronary heart disease, etc.). Thus, the condition of adaptation, adaptation, compensation can be followed essential morfol, the changes and not only stabilized, but also which are steadily progressing. From this it follows that, unlike still eurysynusic idea of primacy of functional changes and secondariness morphological, actually very often functional (clinical) displays of a disease are secondary, i.e. appear only when patol, process already far came in the morfol, registration. Existence preclinical, asymptomatic is also explained by it, the period of a disease, or «predisease», pay to Krom so close attention. Not accidentally and that modern diagnostic methods of diseases — a computer tomography (see. Tomography computer ), ultrasonic diagnosis (see), endoscopy of internals (see. Endoscopy ), routine maintenances of the population (see. Medical examination ), etc. — are aimed first of all at identification of so-called early stages patol, processes when structural changes of bodies already are, but owing to a high level of compensatory and adaptive reactions of an organism they did not become an object of attention of either the most sick, or the doctor yet.




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T. 3. Meerson; V. V. Frolkis (geront.); D. S. Sarkisov.

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