TROPHICITY

From Big Medical Encyclopedia

TROPHICITY (Greek trophe food, food) — the set of processes of food of cells and noncellular elements of various fabrics providing growth, maturing, retention of structure and functions of bodies and fabrics and all organism in general.

T. it is shown in delivery of nutrients to cells and elements of fabrics, utilization of these substances, optimum steadiness of processes of assimilation of simple molecules and dissimilation of the molecules making internal environment of a cell (see Assimilation, Dissimilation), in timely removal of decomposition products and recovery of organic macromolecules (see the Metabolism and energy).

The standard terminology for definition of a trophic condition of an organism, bodies, fabrics and cells: the eutrophia — optimum food, i.e. such relationship between the level of utilization of the nutrients coming to a cell, fabric and body and speed of removal of decomposition products, and also between processes of assimilation and dissimilation of substances, at to-rykh is not observed deviations from their normal structure, physical. - chemical properties and function, to growth potential, development and a differentiation; a hypertrophy — the supernutrition which is expressed increase in weight (see the Hypertrophy) or quantities (see the Hyperplasia) a certain group of cells, or that and another, usually with increase in their function (e.g., fiziol. a hypertrophy of skeletal muscles at their training, a compensatory hypertrophy of one part of pair body after removal of other part); hypotrophy — the subnutrition which is expressed a degrowth (see the Hypotrophy) or quantities (see the Hypoplasia) a certain group of cells, or that and another, usually with decrease in their function (e.g., fiziol. a hypotrophy of skeletal muscles at their divergence, fiziol. a hypotrophy of various fabrics and bodies at the general hypokinesia); an atrophy — lack of food — a gradual degrowth of cells and their disappearance (see the Atrophy); dystrophy the — qualitatively changed, improper feeding bringing to patol. to changes of a structure, physical. - chemical properties and function of cells, fabrics and bodies, their growth, development and a differentiation (see Dystrophy of cells and fabrics). Regional, system and the general distinguish dystrophies.

The diseases of the person and animals which are followed by trophic frustration of their bodies and fabrics, in particular changes of volume, a consistence, the excess or insufficient growth, hypostasis, erosion, ulcerations, a necrosis, etc. are known long since. Also communication between trophic changes of separate bodies and parts of a body was noticed. Still Hippocrates pointed to such communication, noting that «bodies sympathize each other concerning the food». The long time according to the dominating gumoralisti-chesky direction in medicine was considered that fabric trophic disturbances are result of the wrong mixing of natural juice of an organism. The assumption that interference («sympathy — sympathy») internals, at Krom the disease of one of them causes involvement in disease process of other bodies, is carried out «sympathetic», or sympathetic, a nerve for the first time stated to Sh. Vinslou.

In 1824 F. Marangdi in experimental conditions observed at a rabbit trophic disturbances of a cornea of an eye (a so-called neuroparalytic ulcer keratitis) after intracranial section of the first branch of a trifacial. He explained development of an ulcer keratitis after section of a branch of a trifacial with the termination of a flow of a trophic nervous impulsation from c. N of page, cornea, necessary for normal life activity. However Snellen (N. of Snellen, 1857) believed that section of a trifacial conducts to an anesthesia of a cornea and loss of defense reactions by it, as leads to development of inflammatory process. On the other side of Schiff (M. of Schiff, 1867) the main reason for emergence of a keratitis considered the disturbance of blood circulation in front department of an eye which is caused switching off of the vasoconstrictive fibers going as a part of a trifacial.

In 1860 S. Samuel, irritating gasser a node of a trifacial with electric current, showed that development of a keratitis can be observed both at lowered, and at hypersensitivity of a cornea of an eye. It put forward the theory of existence of special trophic nerves: «trophic influence of nerves is that they excite nutritive activity of cells and fabrics. The basis of food lies in cells, its measure consists in trophic nerves». Despite the absence of anatomic data on existence of trophic nerves, this theory a long time used wide recognition though Samuel only considered that there is no «other exit how to allow» or «to establish by an exception» existence of these nerves. Many famous scientists (Sh. Broun-Sekar, Zh. Sharko, I. P. Pavlov, I. Müller, etc.) were followers of this theory. At the same time the cellular theory of R. Virkhov and his followers rejecting a role of a nervous system in disturbances of life activity of fabrics, the doctrine Yu. Kongeyma about value in mechanisms of these disturbances of level of blood supply, and also opening in the field of microbiology and endocrinology of the second half of 19 century gave the chance to explain an etiology and a pathogeny of the diseases which are followed by trophic frustration without attraction of ideas of hypothetical trophic nerves.

However in 1878 Geydengayn found out that the irritation electric current of a drum string or the sympathetic nerve innervating a sialaden causes secretion of saliva, unequal on structure (liquid, with trace amount of organic compounds in the first case, and viscous, rich with organic matters — in the second). As a result of it Geydengayn called a drum string a secretory nerve of a sialaden, and a sympathetic nerve — her trophic nerve, having stipulated, however, that he uses this term only conditionally.

Soon the opinion on existence of trophic nerves was confirmed thanks to I. P. Pavlov's works (1883, 1888) and Gas-kella (W. H. Gaskell, 1883). During the studying of a centrifugal innervation of heart at dogs I. P. Pavlov, analyzing influence of various nerves on heart, allocated two types of nerves — strengthening and weakening. These nerves changed force of cordial reductions, without influencing their rhythm and by that differed from the functional nerves regulating a rhythm of cordial activity. The irritation of the nerve called by it the strengthening nerve of heart was followed by increase in excitability, conductivity and contractility of a myocardium, observed even in the conditions of the termination of blood circulation (on an isolated heart of a hematothermal animal). While the irritation of the accelerating nerve almost constantly involves weakening of cordial activity up to dead stop of body, the strengthening nerve recovers its work. Gaskell, investigating effects of irritation of cardiac nerves of the heart of amphibians which does not have coronary circulation also came to a conclusion that they exert impact on a myocardium by change of a metabolism in it. Sympathetic nerves were called by it catabolic since, in his opinion, they strengthen consumption of nutrients, and nerves of a vagal origin — anabolic, i.e. strengthening processes of assimilation. Gaskell carried the last to trophic. Analyzing the obtained data, I. P. Pavlov came to a conclusion that it is necessary to recognize the strengthening nerve of heart trophic though earlier it inclined that the phenomenon described by it is result of vasodilating influence of a nerve on coronary vessels. The employee of laboratory I. P. Pavlova P. G. Zagradin (1894) showed that the irritation of the strengthening nerve is capable to recover the metabolism in a myocardium broken as a result of influence of Chlorali hydras what recovery of force and heart rate testified to. In his opinion, the accelerating nerves are tied with the nervous device regulating a rhythm of cordial reductions, and the strengthening nerves are related to the myocardium. The irritation of the strengthening nerves increased functional stability of heart while the irritation ослаб^ lyayushchy nerves yielded opposite result.

Further (1922), studying fiziol. mechanisms of activity went. - kish. a path on specially operated animals, I. P. Pavlov repeatedly faced development in them of various trophic disturbances. These disturbances were observed at the operations leading to the considerable shift and a tension of bodies and shown by erosion and ulcerations of skin and mucous membrane of a mouth, a tetany, paresis, etc. I. P. Pavlov considered them as result patol. reflex trophic impacts on bodies and fabrics. On the basis of these data he made the statement that along with the centrifugal nerve fibrils causing functional activity of bodies, and the nerve fibrils which are specially regulating the course of exchange processes exist the vasomotor nerves providing delivery of nutrients to fabrics also. At the same time he meant the sympathetic and parasympathetic fibers operating on a metabolism in mutually opposite direction (see the Autonomic nervous system). They, according to I. P. Pavlov, determine the exact amount of final utilization of the chemical material delivered by blood. Thus, I. P. Pavlov revived the idea forgotten for many decades about a trophic innervation.

JI. A. Orbeli in 1932 — 1949 received the experimental material which allowed it to formulate the doctrine about adaptation and trophic influence of a sympathetic nervous system. In adaptatsionnotrofichesky influence two components inseparably linked among themselves were allocated to them: influences adaptation and influences trophic, the cornerstone of adaptation. Understand such influences of sympathetic nerves as adaptation influences, to-rye lead to changes of functional properties of bodies owing to what there is their adaptation to implementation of these or those functional requirements (see Adaptation). Such shifts come thanks to the fact that sympathetic nerves have the trophic effect which is expressed in change of speed of course of biochemical reactions on bodies.

A concept about adaptation and trophic influences, according to JI. A. Orbeli, «idea of set of those changes which happen in muscular tissue under the influence of a sympathetic innervation and which are expressed, on the one hand, in certain physical and chemical shifts, with another — in changes of functional properties, functional capacities of body» is. These influences which are not connected with change of blood supply extend to all types of cross-striped muscles (see Orbeli — Ginetsinsky a phenomenon), peripheral nerves, receptors, synapses, various departments of c. N of page, hemaden. All effects of adaptation and trophic influence gained at first at irritation - sympathetic nerves, completely are reproduced also irritation of hypothalamic area of a brain — its ergotropny and trofotropny centers from where sympathetic and parasympathetic departments of century of N of page originate (see the Hypothalamus). Thus, in a complete organism adaptation and trophic influences can be carried out as it is reflex (from receptors of esodic nerves), and by direct irritation of the hypothalamic centers, neurons to-rykh participate in formation of autonomic peripheral nerves and to-rye can be excited by the chemical substances which are formed locally or brought by blood.

Orbeli's phenomenon — Ginetsinsky is expressed that tired to full inability to be reduced the skeletal muscle began to answer stimulation of motor nerves after irritation of its sympathetic nerves at first weak, and then with more and more strong reductions. It is noted that at activation of sympathetic nerves the muscle gains developmental potency of stronger tension and its longer maintenance at tetanic excitement (see the Tetanus). JI. A. Orbeli in all this saw analogy to what occurs in heart at irritation of the strengthening nerve of heart in I. P. Pavlov's experiences. The subsequent works which are carried out to JI laboratories. A. Orbeli, showed that in a skeletal muscle at irritation of a sympathetic nerve there is a shortening of its chronaxia (see Hronaksimetriya), simplification of transition of excitement from a nerve to a muscle, sensitization of a skeletal muscle to acetylcholine (see), change of elastoviscous properties and conductivity of a muscle, moderate increase in consumption of oxygen by it and higher extent of its utilization, change of oxidation-reduction processes, an economical expenditure of ATP and strengthening of its resynthesis (see Bio-energetics). In a myocardium under the influence of irritation or section of sympathetic and parasympathetic nerves there are changes of conductivity, oxygen consumption, the maintenance of a glycogen (see), creatine phosphate (see Creatine), ATP, actomyosin (see. Muscular tissue, biochemistry), phosphorus (see), RNA, DNA, phospholipids (see Phosphatides), guanine - adenine - and uracilnucleotides (see. Nucleic acids), changes of activity of a number of enzymes (see) etc.

Adaptation and trophic influence of sympathetic nerves on receptors, on the course of a restitution of esodic nerves, stage of latency and a history of instinctive spinal, vasomotor and respiratory reflexes, and also on uslovnoreflektorny activity is established., These facts are confirmed the assumption of universal value of adaptation and trophic influence of a sympathetic nervous system stated to L. A. Orbeli (1935) since it influences not only all types of muscular tissue, but also fabric formations of other origin while the functional innervation represents the «special case» (superstructure) replacing with itself a role of a local chemical irritant. Adaptation and trophic influence of a sympathetic nervous system, without being starting, modulates the functional act (reception, carrying out, transformation, mediation, excitement, reduction, specific synthesis, secretion, etc.) this or that body also adapts it for requirements of an organism.,

data on ways of transfer of sympathetic incentives on muscle cells are of great importance For understanding of mechanisms of adaptation and trophic influence of sympathetic nerves on a skeletal muscle. In a myocardium of the highest vertebrata the adrenergic device is presented by the three-dimensional network formed by trailer departments of sympathetic fibers that provides direct contacts of these fibers with muscle cells (a direct sympathetic innervation) and bystry achievement in their zone of efficiency concentration of noradrenaline (see). The adrenergic device of skeletal muscles has not a direct bearing on their reduction, performs adaptation function and is constructed by other principle. Its trailer structures do not contact to muscle fibers and are located almost only in an adventitious layer of vessels from where noradrenaline by diffusion on intercellular cracks, and also on a capillary network as

V. A. Govyrin (see t showed. 10, additional materials), arrives to muscle fibers. The ground mass of smooth muscles of a wall of a stomach of mammals, birds and reptiles, a number of hemadens have also no direct sympathetic innervation. Their adrenergic device is located in an adventitious layer of blood vessels. Only io to a measure of thinning of adventitious and muscular layers towards a precapillary zone closer contacts of the terminations with smooth muscle fibers are come and the indirect innervation passes into a straight line. The material basis for performance by adrenergic fibers not only adaptatsionnotrofichesky, but also vasculomotor function is created, thus. Sympathetic nerves exert adaptation and trophic impact on many bodies by means of the pericellular and free bombways (see. Nerve terminations), to-rye have no, however, and is not able to create close contacts with parenchymatous cells of bodies (i.e. cannot be carried to typical synapses) in the zone effective kontsent-r and c iyu but r hell Wren is scarlet in and.

Direct adaptation and trophic impact of a sympathetic nervous system is supplemented with indirect. Results of many researches showed that in the period of relative rest in fluid mediums awake an organismand there is a certain quantity of noradrenaline, to-ry gets to blood, cerebrospinal liquid, a lymph and to intercellular space from the central p peripheral Sinai owls. Its contents significantly increases at fiziol. loadings and extraordinary impacts on an organism. This noradrenaline circulating in fluid mediums of an organism is an important factor of maintenance of T. bodies and fabrics at optimum level or a factor of its disturbance. The proof of possible pathogenic action of noradrenaline is the dystrophy of a myocardium, liver, kidneys and other bodies caused in experiments on animals by introduction by it of high doses of noradrenaline or Reserpinum (S. V. Anichkov of it other, 1969). The second way of indirect adaptation and trophic impact of sympathetic nerves is carried out through the marrow of adrenal glands innervated by preganglionic sympathetic fibers of a big celiac nerve and emitting adrenaline and noradrenaline in blood. These substances of an adrenal origin causing in direct contact with bodies and fabrics the same effects, as well as sympathetic nerves exert impact on different types of exchange and, in particular, on carbohydrate metabolism (see). They strengthen disintegration of a glycogen in a liver that leads to excess accumulation of glucose in blood and its removal with urine. The increased content of glucose in blood is the natural activator of biosynthesis and secretion of insulin. At the same time the tone and excitability of cholinergic system raises and concentration of acetylcholine in fluid mediums of an organism increases.

The third way of adaptation and trophic influence of sympathetic nerves is that noradrenaline which is allocated in fluid mediums of an organism from bombways of these nerves and from marrow of adrenal glands, and also adrenaline arrive through a blood-brain barrier (see) to the hypothalamic area of a brain where, thanks to existence of specific receptors, influence front and back departments of a hypothalamus and its adenogi-pofizotropny zone and by that include in process practically all closed glands, hormones to-rykh possess high biol. activity are also capable to influence all types of a metabolism (see the Metabolism and energy).

The fourth way of adaptation and trophic influence consists that the sympathetic incentives arriving to body for nerves or with the blood containing noradrenaline and adrenaline, changing a trophic condition of fabric education, at the same time change the level of sensitivity of body to hormones. Sensitivity of body to hormones, thus, is a measure of trophic providing substrate and the way regulating effect of these substances.

S. V. Anichkov and his employees (1969) in experiments on animals, irritating reflexogenic zones of an organism and various sites of a hypothalamus, came to a conclusion that the reflex dystrophies of a wall of a stomach developing in these conditions, a liver and a myocardium are caused by the nervous incentives coming to bodies for sympathetic nerves.

Release of a terminalyama of nerves of a large number of noradrenaline under the influence of a high flow of sympathetic impulses and the subsequent exhaustion of stocks of a mediator is a proximate cause of the developing dystrophies. Hormonal factors

in development of these dystrophies, according to S. V. Anichkov, play a supporting role. S. V. Anichkov obtained also data on a possibility of the prevention of neurogenic dystrophies of a stomach, heart and liver by nek-ry neurotropic means.

A. D. Speransky and it sotr.

(1935) in an experiment for receiving neurogenic dystrophies used along with damage of a hypothalamus section sciatic, trigeminal and other nerves and the subsequent irritation of their central and peripheral pieces formalin, croton oil and other chemical substances. Most clearly the picture of neurogenic dystrophies was shown at damage of a sciatic nerve. If the irritation of this nerve was weak, then the disturbances of T revealed macroscopically. were limited to developing of ulcers on a sole of the injured extremity. Brighter picture developed at strong irritation of the central piece of a sciatic nerve. Ulcers developed on an opposite back extremity, front extremities, on slime-sty to a cover went. - kish. path. Along with it dystrophy, pneumonia, nephrite, dystrophic changes of closed glands, and also a spinal cord, a hypothalamus, couple - and prevertebral gangliyev a sympathetic nervous system developed miokar-dio.

A. D. Speransky explained these changes patol. reflex influences, pathogenic character to-rykh was defined not only by power of irritation, but also dystrophies in the most nervous system (nervous dystrophies). Spread of nervous dystrophies to c. out of limits of initially damaged segment led N of page to generalization of process. Localization of primary damage of a nervous system brought distinctions in a picture of neurogenic dystrophies, but mechanisms of their development were same. Therefore the process developing after damage of any site of a nervous system A. D. Speransky called standard neurodystrophic process. Noting the standard party of process and disregarding peculiar features of its manifestation, he wanted to find what combines that makes similar at each other various diseases. He considered that the condition of neurotrophical providing bodies and fabrics is that general background, on Krom peculiar features of a disease develop. To understand a disease — it means to study its trophic component. In these statements there are exaggerations, but time showed that they have some value for the theory and practice.

And. D. Speransky also resolved an issue of existence of special trophic nerves. He wrote: «In relation to processes of neurotrophical character the doctrine about localization can be applied only conditionally... Trophic nervous function per se has no exact localization». It was understood in the sense that any nerve is trophic (any nervous impulse is as well trophic). By analogy with A. D. Speransky H. H. Hare (1966) considered that not trophic nerves do not exist, but ability to influence T. different nerves and the different centers possess not to the same extent.

Functional and trophic components of nervous activity are difficult distinguishable. A. V. Kibyakov (1950) assumed that functional activity of body is caused by the bystry electric discharges proceeding from a nerve whereas T. it is supported by the mediators (acetylcholine, noradrenaline) cosecreted by nerve terminations. A. K. Podshibyakin (1964) distinguished a phase of the fast changings of electric potential in a nerve motivating body to act and a phase of the slow electric potentials directed to recovery of chemical properties of the nerve, and maybe the body innervated by it. P. O. Makarov (1947) allocated the discontinuous (discrete) nervous alarm system which is causing function of body (reduction, secretion), and slitnotonichesky (indiscrete), adjusting body on the new level of activity, i.e. influencing T. Many researchers consider trophic influences as bezympuls-ny and constant, connected with the processes similar to neurosecretion (see). At the same time consider that various substances (corresponding to these or those nerves mediators, particles of mitochondrions, microsomes, kernels and microtubules, peptides and amino acids, DNA, RNA, enzymes, etc.), which are formed in a nervous cell reach executive cells by means of an aksotok (see. A nervous cell), influencing their exchange. Specific activity of body is caused by so-called urgent impulses.

Most of researchers inclines that any nerve possesses trophic function, the same treats also the mediators of nervous excitement circulating in blood. Trophic function of adrenaline, noradrenaline is proved. It is established that serotonin (see) is capable to recover function of the tired muscles and to exert other trophic impacts. It is suggested that have property to change a trophicity of a cell also acetylcholine (see) and a histamine (see).

It is known that the hypothalamus is connected with all departments of c. N of page. Afferent ways connect it with back, oblong and a mesencephalon, a thalamus, basal gangliya, a hippocampus, a rhinencephalon, certain fields of bark of cerebral hemispheres and other structures of a brain. Thanks to such bonds these departments of a brain through a hypothalamus cause all variety of effects of action of century of N of page and hormones according to the alarm system about vegetative events in an organism (including and trophic), edges comes to a brain on afferent nerve pathways, and also a humoral way (in the form of end or intermediate products of a metabolism). Existence of efferent bonds of a hypothalamus with various departments of c. the N of page does possible implementation of nervous and humoral (neurosecretory) hypothalamic trophic influences on various departments of a head and spinal cord. Bilateral ties of a hypothalamus with various departments of c. the N of page speaks influence of a cerebral cortex and other its departments on trophic processes in fabrics, bodies and in an organism in general.

Idea of reflex mechanisms of regulation of T. (trophic reflexes) an organism, for the first time stated by I. P. Pavlov, became almost standard. Feature of a trophic reflex is its slower implementation, than functional reflexes. Therefore in some cases the overstrain of function can be followed by exhaustion of its reserves since ‘the material spent metabolic does not manage to be filled with new. Thus, implementation of function is not supported with immediate trophic providing.

The trophic reflex, as well as functional, consists of an afferent part of a reflex arc, nerve centers and an efferent part. An afferent part (the first link of a trophic reflex) provides receipt on sensory nerves of information on the qualitative and quantitative parties of a metabolism in fabrics in a so-called trophic nerve center. In response to this information the trophic nerve center on efferent pathways directs to the periphery the incentives regulating metabolic rate in body according to requirements imposed to this body at each this moment.

In a wedge, it is noted to practice that trophic frustration arise at damage of sensory nerves more often. A. D. Speransky gave theoretical and experimental justification to these a wedge, to observations. He wrote that any factor promoting strengthening of irritation of a sensory nerve promotes also developing of dystrophy. A. V. Vishnevsky (1928), E. K. Plechkova

(1961), A wrote about a big role of sensory nerves in a pathogeny of neurogenic dystrophies. V. Lebedinsky (1963), etc.

It is supposed that the pathogeny of trophic frustration at damage of sensory nerves is caused by several factors:

1) switching off of an afferent innervation involves loss of information coming in usual conditions to a trophic nerve center on the biochemical changes developing in fabrics; 2) the irritation of a proximal part of the cut nerve arising in it as a result of an inflammation and retrograde degeneration of a part of its fibers. Generated at the same time inadequate patol. incentives come to a trophic nerve center, to-ry includes a cerebral cortex and nek-ry subcrustal structures (a thalamus, a hypothalamus, a reticular formation, etc.), and then on efferent nerves are moved to the periphery, causing still big disturbances of T.; 3) antidromic carrying out on a peripheral piece of a sensory nerve of the impulses of regeneration of this piece aggravating dystrophy on the periphery; 4) an anesthesia of deafferentirovanny body that lowers its protective opportunities; 5) emergence in deafferen-t of pro-bathing fabric of proteins not inherent to it, thanking the Crimea fabric gains autoantigenny properties. The antibodies which are formed at the same time, according to H. H. Hare (1952), can participate in a pathogeny of dystrophies and give them hron. character. Further some more the factors making mechanisms of trophic frustration were allocated.

1) After a degeneration of a peripheral piece of a sensory nerve deafferentirovanny fabric loses all antidromic influences, to-rye are provided usually use-simodistalnym with current of an axoplasm;

2) at the same time receptors collapse, perception of the usual incentives supporting directly local metabolism in receptors stops; and the cells surrounding them that is capable to strengthen dystrophy of deafferentiro-bathing fabric; 3) as the full deafferentation of fabrics is impossible, the arising dystrophic changes on the periphery act as a source of long unusual irritation ekstero-and (or) interoceptors of the remained afferent fibers, a cut is the additional reason of inadequate answers of fabric; 4) section of an esodic nerve leads to dystrophic changes of sensory cells gangliyev and the centers back and a brain, the T which are carrying out regulation. corresponding fabrics. Dystrophy of nervous cells breaks processes of transformation of the signals passing through the centers to deafferentiro-bathing fabric for efferent nerves and by that promotes a bigger damage of its structure and function; 5) set of the above-stated factors, breaking T. fabrics, leads to change of its sensitivity to direct nervous and humoral influences; 6) the deafferentation sharply breaks a tone of blood vessels of fabric and by that worsens its blood supply, change to-rogo promotes not only to strengthening of dystrophy of cells, but also their death; 7) the abnormal impulsation, coming from a proximal stump of a sensory nerve, reaches a front and back hypothalamus, and also its adenogipofi-zotropny zone, breaking functional activity of closed glands and concentration of the hormones in an organism having ability to change food of fabrics; 8) damage of an esodic nerve leads to change of concentration of the mediators of nervous excitement circulating in the fluid mediums of an organism influencing T. deafferentirovanny fabric directly or indirectly.

Existence of the listed factors making pathogenetic mechanisms of neurogenic dystrophies is confirmed by numerous researches. This scheme of a pathogeny of trophic frustration, perhaps, does not reflect all its complexity, but demonstrates that the theories which are based on one of the listed factors of pathogenetic mechanisms of neurogenic dystrophies will not be able to give effective ways of treatment of the dystrophies arising owing to a deafferentation of fabric.

It is necessary to consider that in the conditions of a deefferentation fabric loses only normal trophic influences whereas at a deafferentation patol. it is much more essential than an effect. At the mixed denervation of fabrics the factor of loss of efferent nervous influences is added to listed — fabric loses direct nervous stimulation of cells of its parenchyma and a stroma on accessory fibers, and also the nervous influences mediated by changes of local blood circulation as the mixed denervation is always followed by damage of vasomotor nerve fibrils, a cut causes paresis of blood vessels, formation of blood clots, a hemostasis, change of permeability of a vascular wall, swelled also infiltration of fabrics leukocytes.

The nerve trophic center (the second link of a trophic reflex) represents system of various, but closely connected among themselves by afferent and efferent pathways departments back and a brain, including a hypothalamus. Direct impacts on these departments of a brain, napr, the sugar prick offered by K. Bernard, the operation of a ball executed by A. D. Speransky, the removal of bark of big hemispheres made by B. I. Bayandurov, functional weakening of a cerebral cortex as a result of an overstrain of its function, etc., is led to disturbance of T. on the periphery.

The third link of a trophic reflex is presented by efferent nerves, hormones and mediators of nervous excitement. Carry both somatic, and autonomic nerves to efferent trophic nerves. Though trophic function of a sympathetic nerve is proved, his irritation or section not always lead to dystrophic shifts. At absence or deficit of nervous incentives it is explained by the compensating action of catecholamines (see) fluid mediums of an organism (a so-called liquid simpatikus). However at intensive impact on a sympathetic nervous system (e.g., owing to damage of a hypothalamus, crush of an upper cervical sympathetic node, damage of nodes of an abdominal brain, etc.) dystrophies arise. The phenomenon use of an imodistalny aksotok in sensitive fibers is considered as one of mechanisms of efferent influence of esodic nerves on T.

Hormones (see) and mediators (see) nervous excitement, allocated by a nervous system in fluid mediums of an organism and components the third link of a trophic reflex, influence metabolism of fabrics, especially those, to-rye undergo dener-vatsionny and reflex dystrophies as trophic shifts in fabrics of any origin sharply change sensitivity of fabric substrate to effect of hormones and a number of nesinaptichesky mediators (noradrenaline, acetyl-holpn, serotonin, GAMK, a histamine). This phenomenon concerning denervprovanny structures is established by U. Kennon and Rozenblyut (A. S. Rosenblueth, 1951). On the fabrics enduring reflex dystrophies it is studied by Ya. I. Azhipa (1970, 1981) p it sotr. In particular, it is shown that shifts of sensitivity to hormones and mediators of fabrics and bodies at their reflex dystrophy or a compensatory hypertrophy are connected both with damage of specific receptor devices, and with disturbance of intracellular nonspecific metabolism. At the same time, apparently, patol. both weakening of specific reception and its strengthening can be the beginning. Deficit of neurotrophical influences can lead to pathogenic relationship between hormones and fabric, being followed by structural changes of fabric up to its malignant regeneration. An example as Biskind and Biskind (M. of S showed. In island,

G. R. Biskind, 1944), Li and Gardner (M. S. of Li, W. U. Gardner, 1947), etc., can serve cystous, and then tumoral regeneration of completely denervated ovary differing markedly a hyposensitivity to gonadotropic hormones (see) in the conditions of the increased contents them in an organism caused by removal of other ovary. The conclusion was drawn that disturbance adaptation trophic go influences of a nervous system on fabrics negatively influences the adaptive reactions allowing fabrics to resist to long influence of surplus or a lack of hormones and by that promotes transformation of this or that hormone into a disturbing factor.

The terminations of autonomic nerves are located in various bodies in relation to parenchymatous cells p to other fabric elements differently. In a myocardium, e.g., one nerve terminations of adrenergic and holinergnchesky nerves approach directly an endothelium of capillaries or their pericytes, others — myocytes of body, the third — innervate at the same time both capillaries, and parenchymatous cells, the fourth — are located freely in intercellular space. In a number of bodies of the termination of autonomic nerves are localized in an adventitia of blood vessels or in intercellular intervals. Nek-ry fabrics are not provided with nerves at all. Despite such variety of localization of nerve terminations of autonomic nerves, all cells in all fabrics come under neurotrophical influence. It is connected with the fact that the main way of nervous control of such fabric educations is delivery of neurotransmitters to cells (on nesinaptichesky type) and their subsequent diffusion in the direction of a microvascular bed and intercellular space, i.e. to those structures, to-rye make morfol. a basis of microcirculation (see). At the same time the distance from nerve termination to parenchymatous cell is of great importance. It defines the direct (immediate) or indirect (slowed-down) nervous control of T. cells.

In 1975 A. M. Chernukh made a hypothesis that nervous control of T. fabrics, microcirculation and transcapillary exchange are uniform integral process of any functional element of body.

Along with system of microcirculation in mechanisms of implementation of adaptation and trophic function of a nervous system an important role is played, apparently, by intercellular contacts of parenchymatous cells among themselves and with structural elements of connecting fabric. In many cases these contacts are made by means of physiologically active agents, to-rye are released from the adjoining cells under the influence of neurotransmitters and hormones. End and intermediate products of a nonspecific metabolism, mediators, or modulators, cyclic nucleotides, prostaglandins, etc. can act as such substances. Communication between cells by means of elaborate contacts is proved, the structure to-rykh adequately corresponds to features of the functional organization of fabric. Are widely studied physical. - chemical, supramolecular and subcellular properties of intercellular contacts. Are found, but the substances participating in mechanisms of adhesion, diffusion and barrier functions still are in details chemically not identified. Many-sided variability of the structures defining intercellular contacts under the influence of factors of surrounding and internal environments of an organism is shown. At the same time influence on these contacts of physiologically active agents is still a little studied. There are only data on effect on them of concanavalin, salicylates, calcium ions, lanthanum, nek-ry complexons, an auratina, Prednisolonum, factors of aggregation and adhesion (proteoglycans, glycoproteins), thyroxine. The fact that intercellular contacts play an important role in processes of an embryogenesis, regeneration, tumoral growth, etc. indicates their participation in T. cells in itself. The facts speaking about change of durability of intercellular contacts and a stseplennost of cells under the influence of nek-ry hormones, acetylcholine, Carbacholinum and about tsaru-sheniye of their structure at the stressful impacts on an organism which are followed obrazovaniyekhm ulcers in a mucous membrane of intestines demonstrates that the nervous system uses intercellular interactions between homogeneous and diverse cells for implementation of the adaptatsionnotrofichesky influence on bodies and fabrics. If to consider action of the mediators of nervous excitement circulating in blood on the cells which are not adjoining to nerve terminations and value for T. contacts of these cells with the cells connected with nerve fibrils classical synapses, there is more clear a mechanism of adaptatsionnotrofichesky influence of a nervous system on the cell populations which do not have nerves.

In a cell transmitters of adaptation and trophic influence of mediators of nervous excitement are the special receptors of mediators which are built in a membrane of cells, adenylatecyclase, cyclic a 3,5-a denozpnmonofosfat, cyclic 3,5-guanozinmonofos-veils (see Receptors, cellular receptors). Each mediator adenylatecyclase — cyclic AMF or cyclic GMF by means of primary contact with the specific receptor separately activates system (see). So, catecholamines activate adenylatecyclase through R-adrenoceptors. Noradrenaline brought by in vitro to a hypophysis of a rat causes strengthening of cyclic AMF several times. The hypophysis which is previously deprived to a simpaticha

of a sky innervation, and then allocated from an organism has hypersensitivity to noradrenaline on the same indicator by 5 times. As noradrenaline activates

in a desimpatizirovanny hypophysis of animals adenylatecyclase more than in intact body, without exerting impacts on phosphodiesterase, it is possible to assume that similar sensitization of a hypophysis is a consequence of strengthening of synthesis of cyclic AMF, but not reduction of its disintegration. It is possible that such changes in concentration of tsAMF after a denervatsna play a compensatory role.

The special group of physiologically active agents — oligopeptid is allocated. Carry the fragments of AKTG, analogs of vasopressin and oxytocin, a liberina identified at different times, somatostatin, enkephalins, endorphines, substance P, angiotensin II, bradykinin to them, r-lipotropin, neyrotenzin, gastrin, cholecystokinin, their derivatives and other peptides (see). These substances are called neuropeptids (see the Neurochemistry) as they are capable to modulate effects of mediators at the presynaptic and postsynaptic level, to influence their synthesis, removal and disintegration, interaction with each other. Besides, nek-ry of them perform function of mediators in peptpde-rgichesky synapses. Nek-ry oligopeptida have high ability to get into a nervous cell — up to a kernel, and on an axon — before the synoptic termination. There are this, testimonial of communication of intracellular effects of a number of peptides with and Denis l at-tsiklazny system and prostaglandins. Biol. effects of neuropeptids are extremely diverse. They affect mechanisms of memory, training, behavior, emotions, painful sensitivity, function of closed and excretory glands, action of the heart, kidneys, went. - kish. path etc. There are no faultless data on participation of neuropeptids in implementation of trophic function in the methodical relation of a nervous system yet, but the listed above facts allow to consider that these substances play a significant role in implementation of neurotrophical function and as mediators of peptidergichesky neurons, both modulators of action of neurotransmitters, and the substances regulating function of hemadens, and the factors providing both mezhneyronalny, and inside-neyronalnuyu integration of qualitatively various incentives coming to separate neuron (see. Nervous cell).

Trophic disturbances — pathological physical. - chemical and morfol. the changes in cells and fabrics which are a consequence of disturbance of delivery of nutrients to cells and elements of fabric, utilization of these substances, processes of their assimilation and dissimilation, and also processes of removal of end and intermediate products of a metabolism of cells and fabrics.

Distinguish the general, the system, regional, acquired and inborn trophic disturbances. More often they are a symptom of a disease, is more rare — independent nozol. form. Allocate trophic frustration, to-rykh are the reason complete, incomplete and high-quality starvation (see), disturbance of blood circulation (see) and immunoal-lergichesky reactivity of an organism (see the Immunopathology), intoxication (see), infections (see), ionizing and Uv-radiation (see. Ionizing radiation, Ultraviolet radiation), ultrasound (see), vibration (see), zero gravity (see), diseases of closed glands and a nervous system, disturbance pre-natal, pre-and post-natal development, connected with defects of the hereditary device (see. Hereditary diseases).

The complete starvation is followed by dysfunction of all cells and body tissues. Fatty tissue disappears completely. Muscles, losing at first carbohydrates, and then fats and proteins, decrease in weight. Also the weight of a spleen, pancreas, liver, heart, adrenal glands decreases, in a smaller measure structures of a head and spinal cord suffer. Reduction of weight of bodies goes not only at the expense of an expenditure of nutrients, but also due to death of cells.

Incomplete starvation, as a rule, «drags on» in time owing to what dystrophic changes develop gradually and are more diverse (see Dystrophy of cells and fabrics). In the beginning they come to light only by means of physical. - chemical indicators, and then they are found macroscopically.

At patients with a nutritional dystrophy are broken thermoregulation, the main, nitrogenous, carbohydrate, fatty, water-salt, vitamin and other types of exchange, there are hypostases. The susceptibility to inf raises. to diseases. Children have a growth inhibition, mental development, there are hypostases, a dermatosis, anemia, synthesis of protein is broken and activity of enzymes falls, the weight and quantity of cells in bodies decreases, fatty dystrophy of a liver is observed, disturbance of nutritive absorption in went. - kish. path.

Complete or partial vitamin starvation (avitaminosis, hypovitaminosis) is characterized by disturbances of various links of a metabolism. Hypovitaminoses are shown in the form of sharp falling of body resistance to inf. to diseases, considerable decrease in working capacity, body weight. At children lag in growth is noted. At nek-ry pshovitaminoza local dystrophies develop (ssh. Vitamin deficiency).

Trophic disturbances can be a consequence of insufficient receipt in an organism of irreplaceable amino acids (see Amino acids). E.g., the exception of a diet of tryptophane leads at rats to vascularization of a cornea and a cataract. Absence in food of arginine oppresses a spermatogenesis (see), and the lack of a histidine is followed by decrease in concentration of hemoglobin. The exception of food of methionine is followed by fatty dystrophy of a liver. The lack of valine conducts to a growth inhibition of animals, a lose of weight (weight) of a body, development of keratoz. The lack of nek-ry replaceable amino acids can be also followed by disturbances T. Tak, deficit of cystine leads to growth inhibition of cells even in the presence of all other amino acids. At cats the lack of taurine leads to dying off of photoreceptor cells of a retina of an eye.

As at complete, incomplete and high-quality starvation (primary or secondary) function and a trophicity of nervous and endocrine systems suffer, it is possible to consider that neurodystrophic and hormonal components take part in a pathogeny of trophic frustration at starvation.

The general, system and local disturbances of blood circulation are the frequent reason of dystrophic changes (see). Complete cessation of blood supply of fabrics leads to their necrosis (see). Hron. reduction of inflow of blood (i.e. long poor supply of body nutrients, including oxygen) is followed by disturbance of an intracellular metabolism, reduction of the sizes of cells, necrotic shifts in them and their death. As a result such states as dystrophy of a myocardium, liver, kidneys, disintegration of certain sites of nervous tissue, a hypotrophy of closed glands, an atrophy of muscular tissue, thinning of skin or a hyperkeratosis, erosion, ulcers, gangrene of extremities (develop at generalized or regional atherosclerosis, an endarteritis, a prelum of arteries). Difficulty of outflow of a venous blood is followed by discoloration of body (cyanosis, cyanosis), hypostasis, death of a parenchyma of body, growth of connecting fabric, to Indus radio set of bodies. In clinic angioneuroses — angiotrofonevroza are allocated (see), at to-rykh disturbance of exchange and food of fabrics takes place. Carry an acroparesthesia, a Crocq's disease to them (see), an erythremegalia, a Raynaud's disease (see Reynaud a disease), a Quincke's disease — Quincke's disease (see Quincke swelled), etc.

Trophic disturbances accompany nek-ry allergic reactions of an organism. At a serum disease are observed a hyperplasia limf, nodes, urticaria, erythematic rash with an itch, often a face edema, joints. The pollinosis (hay fever) is followed by rhinitis, conjunctivitis, razdrazheniyekhm and an itch a century, and in hard cases bronchial asthma. At classical bronchial asthma hypostasis of a slizistonbolochka of bronchial tubes develops, hypersecretion of mucous glands of bronchial tubes is observed.

Trophic frustration at the general and local impact of ionizing radiation are various (see. Ionizing radiation, Radiation). They are presented by an erythema, bubbles and ulcers, hypostasis, a necrosis, multiple hemorrhages on skin, to a mucous membrane of a mouth, a gullet, a stomach, intestines etc. (see. Radial illness).

Hron. poisoning with alcohol leads to sclerous changes in a liver, heart and other bodies (see an alcoholism). Methyl alcohol (see) causes regeneration of nervous tissue, especially visual analyzer, perchloromethane (see) — a necrosis of cells of a liver; trophic disturbances cause also other chemical substances (see Poisonings).

The increase or reduction of concentration of hormones in an organism caused by diseases of closed glands or changes of their function at extraordinary influences often are followed by disturbance of T. general, system, or local character. Functional insufficiency of a hypophysis or its removal leads to an atrophy of a thyroid gland, bark of adrenal glands and gonads that in turn causes jumps of all types of exchange in fabrics and bodies (see the Hypophysis). Insufficient allocation of a growth hormone (see. Somatotropic hormone) is the main reason for a Lorain's disease (see). Decrease in secretion of thyritropic hormone (see) leads to development of a hypothyroidism and a mix of Dyoma, at to-rykh the expressed changes of T are noted. an organism (see the Hypothyroidism). The lack of gonadotropic hormones (see) causes disturbances of secretion of sex hormones in this connection can develop a prepubertatny eunuchoidism, infantility with a growth inhibition of an organism and an adiposagenital syndrome, the reason a cut consider primary defeat of a hypothalamus, etc.

Diseases of a thyroid gland are also characterized by considerable trophic frustration. The inborn aplasia of gland results in cretinism (see). The thyroid insufficiency acquired in the childhood or youth is followed by a myxedema (see). The increased function of a thyroid gland and especially a thyrotoxicosis (see) also lead to trophic frustration. They are observed

in l. - kish. path, liver, endocrine glands and other fabrics and bodies. Trophic shifts in the whole organism and in its separate bodies and fabrics take place also at diseases of gonads, bark of adrenal glands, an incretory part of a pancreas, epithelial bodies, an epiphysis, damage of S-cells of a thyroid gland (see. Endocrine system).

In an experiment on animals it is established that long increase in maintenance of mediators of nervous excitement in fluid mediums of an organism, and also in bodies and fabrics can be a proximate cause of trophic disturbances. So, at wound of a sciatic nerve hron. back extremity ulcers contain a large number of acetylcholine (see). Introduction by an animal of adrenaline (see), noradrenaline (see), dopamine (see Catecholamines) and Reserpinum (see) in high doses causes dystrophy of a myocardium, liver, kidneys and other bodies. High doses of serotonin caused formation of stomach ulcers in animals. Increasing permeability of capillaries, serotonin (see) participates in development of hypostases, including and allergic. In this respect it is much more active than a histamine (see). Locators of monoaminergiche-sky receptors would prevent or limited development of dystrophies.

Trophic disturbances at injury of various parts of the nervous system are diverse, especially at extensive injuries or irritation of the large mixed nerves. In such cases trophic disturbances are observed in all fabrics, bodies and systems, including in nervous and endocrine systems. Limited injuries of the central and peripheral parts of the nervous system are followed by regional trophic frustration, character to-rykh is defined by specifics of the damaged site of a nervous system and the innervated body or fabric.

Differential diagnosis of trophic frustration in the most nervous system and their directed therapy are based on two types of classification.

One of them is based on the loka-lpzatsionny (system) principle and allocates trophic disorders of a cerebral cortex and subcrustal structures, pyramidal ii extrapyramidal systems, a brainstem, a myelencephalon and cranial nerves, a diencephalon, a sgshnny brain etc. It is known St. 2000 reflexes, reactions, symptoms, syndromes, tests, receptions, with the help to-rykh make definition of localizations of organic lesions of a nervous system. Classification by the localization principle is supplemented by classification of nervous dystrophies on etiol. to a sign. Carry to the reasons of trophic frustration of nervous tissue: infections, ekzo-

II endogenous intoxications; vascular frustration (strokes, hemorrhages, ischemia, etc.); tumors of various origin, localization and current; bruises; impact of ionizing radiation; hypokinesia; primary injuries of bones, joints, ligaments of a skull, backbone and basin; the disturbances of pre-natal and post-natal development connected with defects of the hereditary device (a spastic rachioplegia, hron. the progressing ataxy, a chorea of Gentington, a hepatolenticular degeneration, an atrophy of optic nerves, an amaurotic idiocy, an aplasia of subcrustal white matter of parencephalons, nek-ry forms of degenerative changes of a cerebellum), etc.

Many disturbances of T. nervous tissue of a head and spinal cord, and also a peripheral nervous system lead to disturbance only functions of peripheral bodies, others are followed by neurogenic dystrophies. These dystrophies are shown in the form of disturbances proteinaceous, nucleinic, fatty, carbohydrate and other types of exchange; muscular dystrophies, amyotonias, myasthenias, atrophy, thickening, peeling, hypostasis, hyperpegmentation, not healing cracks and grazes, erosion, decubituses, eczemas, ulcers of skin; atrophies or fragilities of nails; phlegmons, pyodermas, furunculosis; atrophies of sheaves, perversions of growth of bones, osteomalacy, spondiloz, spondylarthrosis, sclerosis and anchylosis of joints; contractures of aponeuroses; gastritis, erosion, stomach ulcers, gullet and intestines; inborn heart diseases, hypotrophy of closed glands etc. In case of extensive organic lesions in the field of a diencephalon and gi-potalamo-pituitary system various trophic frustration in peripheral bodies and fabrics develop.

The inborn dystrophies forming in the pre-natal period under the influence of adverse exogenous and internal causes (toxicoses of pregnant women, pharmaceuticals, professional harm, rheumatism, hron. pneumonia, pyelonephritis, anemia, etc.), divide into four a wedge, forms: neuropathic, it-rodistrofichesky, neuroendocrinal and encephalopathic. The same factors of an exogenous and endogenous origin can lead to limited disturbances of embryonic development with local defects of separate fabrics, bodies and systems.

In some cases it is difficult to distinguish inborn dystrophies from inherited disorders of T., to-rye can be shown at all stages of ontogenesis, including and in the embryonal period and therefore, right after the birth (see. Hereditary diseases). One hereditary diseases are shown in the childhood, and others — at mature or advanced age (e.g., gout develops after 35 — 50 years). Hereditary dystrophies are known, to-rye connect with disturbance of a certain type of a metabolism or with I izkhmeneni-eat activities of a certain enzyme: muscular dystrophies like Dyushenn, a spherocytosis, an adiposagenital syndrome, a disease Andersen (cirrhosis), a disease to the Pomp (a glycogenosis of heart), cretinism, Gerke's disease (a generalized glycogenosis) etc. Hereditary diseases of blood, to-rye are connected with disturbance of exchange of hemoglobin, enzymes and proteins of plasma, it is also possible to carry to trophic frustration. A number of inherited trophic disorders carry to the frustration of a secondary order which are a consequence of primary hereditary diseases of nervous and endocrine systems.

Trophic changes in advanced and senile age take nervous, endocrine, digestive, muscular, cardiovascular, respiratory systems, skin and its appendages, a skeleton, kidneys, sense bodys (see the Old age, aging). The general for all fabrics and bodies is death of cells without recovery (the post-mitotic cells which lost ability to division) or reduction of speed of cell fission, delay of their updating, increase of duration of a cellular cycle, increase in body of quantity of old cells (the premitotic cells keeping ability to division). In that and other case dystrophy of fabric structures accrues and their functional activity decreases. Intensity of all types of a metabolism changes.

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