BLOOD LOSS — the pathological process resulting from damage of vessels and loss of a part of blood, which is characterized by a number of pathological and adaptive reactions.
The etiology and a pathogeny
is of Prichina K. bleeding (see), a cut it can be caused by wound of blood vessels, patol, process (stomach ulcer, intestines, atherosclerosis of large vessels, a tumor, tuberculosis, a varicosity etc.), a disease of capillaries; a specific place is held by disturbance of coagulant system of blood, then insignificant damage of a vessel can lead to deadly K. V to obstetric practice To. it is possible at pathology of childbirth, at an atony of a uterus after the delivery and other complications (see. Childbirth ).
Fiziol. To. it is observed at periods, during normal childbirth and it is easily compensated by an organism.
Patol. To., as a rule, demands medical intervention.
Changes at To. it is conditionally possible to divide into several stages: initial, stage of compensation and terminal. As the releaser causing compensatory and patol, changes in an organism as a result of a loss of blood serves reduction of the volume of the circulating blood (VCB). Priming reaction on a loss of blood is the spasm of small arteries and arterioles resulting reflex from irritation of receptor vascular zones and increase in a tone of a sympathetic part of century of N of page. Thanks to it, even at a big loss of blood if it proceeds slowly, datum level of the ABP can remain. Reduction of a gleam of small arteries and arterioles leads to increase in the general peripheric resistance increasing according to increase in mass of the lost blood and decrease in OTsK that, in turn, leads to reduction of a venous inflow to heart. Reflex increase of a cordial rhythm in an initial stage To. in response to reduction of the ABP and change of chemical composition of blood some time supports cordial emission, but further it steadily falls (in experiences on dogs at extremely heavy To. reduction of cordial emission by 10 times at simultaneous falling of the ABP in large vessels to 0 — 5 mm of mercury was registered.). In a stage of compensation, in addition to increase of a cordial rhythm, force of reductions of heart increases and the amount of residual blood in ventricles of heart decreases. In an end-stage force of cordial reductions decreases, residual blood in ventricles is not used.
At To. changes funkts, the condition of a myocardium, decreases the most achievable speed of reduction. Reaction of coronary vessels on To. has the features. Right at the beginning To., when the ABP decreases at a small size, the volume of a coronary blood-groove does not change; in process of falling of the ABP also the volume of a blood-groove in coronary vessels of heart, but to a lesser extent, than the ABP decreases. So, at decrease in the ABP to 50% of initial level the coronary blood stream decreased only by 30%. The coronary blood stream remains even during the falling of the ABP in a carotid artery to 0. Changes of an ECG reflect the progressing hypoxia of a myocardium: in the beginning increase of a rhythm is noted, and then, at increase in a loss of blood, its delay, decrease in a voltage of a tooth I, inversion and increase in a tooth of T, decrease in a segment S — T and disturbance of conductivity up to emergence of cross blockade, blockade of legs of an atrioventricular band (ventriculonector), an idioventricular rhythm. The last matters for the forecast as degree of co-ordination of cardiac performance depends on function of conductivity.
There is a redistribution of blood in bodies; first of all the blood stream in skin, muscles decreases, maintenance of a blood-groove in heart, adrenal glands, a brain is provided to these. G. I. Mchedlishvili (1968) described the mechanism allowing to support in a brain short time the reduced blood circulation even at decrease in the ABP in large vessels to 0. In kidneys there is a redistribution of a blood-groove from cortical substance in brain as the juxtaglomerular shunt (see. Kidneys ), what leads to delay of a blood-groove since in marrow it more slowly, than in cortical; the spasm of interlobular arteries and afferent arterioles of balls is observed. At decrease in the ABP to 50 — 60 mm of mercury. the renal blood stream decreases by 30%. Considerable disturbances of blood circulation in kidneys cause decrease in a diuresis, and falling of the ABP is lower than 40 mm of mercury. leads to the termination of an uropoiesis since hydrostatic pressure in capillaries becomes less oncotic pressure of plasma. As a result of falling of the ABP the periarterial pad of kidneys strengthens secretion renin (see), and its content in blood can increase to 5 times. Under the influence of a renin it is formed angiotensin (see) which narrows vessels and stimulates secretion Aldosteronum (see). Decrease in a renal blood-groove and disturbance of filtering is observed within several days after the postponed K. Ostraya renal failure (see) can develop at heavy To. in case of overdue and incomplete substitution of the lost blood. The hepatic blood stream decreases parallel to falling of cordial emission.
Blood supply of fabrics and the ABP a nek-swarm time can be supported due to redistribution of blood in vascular system and transition of a part it from a low-pressure system (a vein, a small circle of blood circulation) in system of high. Thus reduction of OTsK to 10% without change of the ABP and cardiac performance can be compensated. As a result a little venous pressure decreases. Favorable action of bloodlettings at venous zastoyakh and hypostases is based on it, including at a fluid lungs.
Frustration microcirculation (see) in an initial stage occurs due to disclosure of arteriolovenulyarny shunts: owing to a spasm of precapillary sphincters of nek-paradise a part of blood, passing capillaries, passes through an anastomosis in venules, blood supply of skeletal muscles as a result worsens, but return of blood to heart (centralization of blood circulation) is facilitated. During the falling of the ABP it is lower than 50 mm of mercury. blood accumulates in capillaries, the speed of its movement is slowed down, the pendulum movement is observed, in separate capillaries comes staz, the number of the functioning capillaries is reduced. Some capillaries are filled almost only with plasma, and others — units of erythrocytes. In an end-stage in separate capillaries formation of microblood clots is observed. Further microcirculation disorder to irreversible changes in bodies and secondary insufficiency of heart.
A hypoxia at To. has circulator character, and degree of its expressiveness depends on weight of disturbance of a hemodynamics. At loss no more than 10 ml/kg of blood oxygen consumption is not broken, the respiratory rhythm is not changed or speeded up. At further bleeding cordial emission falls, oxygen consumption decreases, the respiratory rhythm is broken and oxygen dissotsiatsionnaya the curve moves to the right and down that facilitates return of oxygen in capillaries (see. Gemoglobin ). Considerably arteriovenous distinction on oxygen and coefficient of utilization of oxygen fabrics increases.
Arteriovenous distinction at heavy To. makes 10 — 12 about. % (is normal 5 — 6 about. %). Saturation of aterialny blood oxygen remains normal that is connected with increase in lung ventilation. At the beginning To. increase in arteriovenous distinction compensates reduction of system transport of oxygen, but further in connection with strong reduction of cordial emission oxygen consumption decreases and the heavy hypoxia with defeat of c develops. N of page (see. Hypoxia, hypoxia of a brain ).
Tension of oxygen (pO 2 ) changes in an arterial blood a little and it is strong — in venous; at heavy To. pO 2 falls from 46 to 23 mm of mercury., and in blood of a coronal sine from 21 to 12 mm of mercury. Changes of pO 2 reflect the nature of supply with their blood in fabrics. In an experiment in skeletal muscles of pO 2 the ABP decreases quicker, than; pO 2 in a wall of a small bowel and a stomach decreases parallel to decrease in the ABP. In bark and subcrustal nodes of a brain, and also in a myocardium decrease in pO 2 it is slowed down in comparison with decrease in the ABP.
For compensation of the phenomena of a circulator hypoxia in an organism there is a following: 1) redistribution of blood and preservation of a blood-groove in vitals due to reduction of blood supply of skin, digestive organs and, perhaps, muscles; 2) recovery of volume of the circulating blood as a result of inflow of an interintercellular lymph to a blood channel; 3) increase in cordial emission and coefficient of utilization of oxygen at recovery of volume of the circulating blood. Two last processes promote transition of a circulator hypoxia in anemic, edges constitutes smaller danger and is easier compensated.
The hypoxia of fabrics developing in time To., leads to accumulation in an organism of nedookislenny products of exchange and to to acidosis (see) which has the compensated character in the beginning. During the deepening To. noncompensated acidosis with decrease in pH in a venous blood to 7,0 — 7,05, and in arterial — to 7,17 — 7,20 and falling of alkaline reserves develops. In an end-stage To. acidosis of a venous blood is combined with an alkalosis arterial (see. Alkalosis ); at this pH in an arterial blood does not change or slightly moves in the alkaline party, but the content and tension of carbon dioxide gas significantly decreases (pCO 2 ), what is connected as with falling of pCO 2 in an alveolar air as a result of the strengthened ventilation of the lungs, and with destruction of bicarbonates of plasma. At the same time the respiratory coefficient becomes more than 1. Blood loss
is resulted by fluidifying of blood; decrease in OTsK is compensated by an organism by receipt in a blood channel of liquid from interfabric spaces and the proteins dissolved in it (see. Hydremia ). At the same time the system a hypophysis — cortical substance of adrenal glands becomes more active; secretion of Aldosteronum which strengthens a reabsorption of sodium in proximal department of renal tubules increases. The delay of sodium leads to strengthening of a reabsorption of water in tubules and to reduction of an uropoiesis. At the same time the content in blood of antidiuretic hormone of a back share of a hypophysis increases. In an experiment it is established that after very massive To. recovery of volume of plasma happens quickly enough and within the first days its volume surpasses initial size. Recovery of proteins of plasma goes to two phases: in the first phase during the first two-three days it occurs due to mobilization of fabric proteins; in the second phase — as a result of strengthening of protein synthesis in a liver; the complete recovery comes in 8 — 10 days. The proteins which came to a blood channel have qualitative difference from normal serum proteins (they have the increased colloid and osmotic activity testimonial of their bigger dispersion).
The hyperglycemia develops, the maintenance of a lactate dehydrogenase and aspartate aminotransferase increases in blood that indicates damage of a liver and kidneys; concentration of the main cations and anions of plasma a shelter of the item changes. At To. the caption of a complement, pretsipitin and agglutinins decreases; sensitivity of an organism to a tank - those to yards and their endotoxins increases; phagocytosis is suppressed, in particular phagocytal activity of kupferovsky cells of a liver goes down and remains to the blood broken several days after recovery of volume. However it is noted that small repeated bleedings increase development of antibodies.
A blood coagulation at To. accelerates, despite reduction of number of thrombocytes and content of fibrinogen. At the same time fibrinolitic activity of blood increases. Increase in a tone of a sympathetic part of century of N of page and the strengthened emission of adrenaline, undoubtedly, promote acceleration of a blood coagulation. At the same time changes in components of coagulant system are of great importance. The platelet stickness and their ability to aggregation, consumption of a prothrombin, concentration of thrombin, the maintenance of the VIII factor increase, the content of anti-hemophilic globulin decreases. With an interintercellular lymph thromboplastin, from the destroyed erythrocytes — an anti-heparin factor arrives fabric (see. Coagulant system of blood ).
Changes in system of a hemostasis remain within several days when the general blood clotting time is already normalized. Recovery of number of thrombocytes after a loss of blood goes very quickly. In to a leukocytic formula (see) the leukopenia with a relative lymphocytosis, and then a neutrophylic leukocytosis which has redistribution character in the beginning is found in the beginning, and then it is caused by activation of a hemogenesis what the deviation to the left testifies to.
The quantity of erythrocytes and a hemoglobin content decrease depending on the volume of the lost blood, at the same time the major role is played by the subsequent cultivation of blood an interintercellular lymph. The minimum concentration of hemoglobin necessary for maintenance of life at recovery of volume of blood makes 3 g of % (in experimental conditions). The absolute quantity of erythrocytes continues to decrease also in the posthemorrhagic period. During the first hours after a loss of blood contents erythropoetins (see) decreases, then in 5 hours begins to increase. The largest content them is observed on the 1st and 5th days. To., and the first peak is connected with a hypoxia, and the second matches activation of marrow. Recovery of composition of blood is promoted also by strengthening of formation of an internal factor of Kasl in a mucous membrane of a stomach (see. Kasla factors ).
Nervous, endocrine and fabric factors take part in implementation of compensatory reactions. The cordial and vascular reactions leading to redistribution of blood arise reflex at irritation of receptor zones (sinocarotid and aortas). Excitement of a sympathetic part of century of N of page conducts to a spasm of arterial vessels and tachycardia. Function of a front share of a hypophysis and adrenal glands amplifies. Emission increases catecholamines (see), and also content in blood of Aldosteronum, renin, angiotensin. Hormonal influences support a vasospasm, change their permeability and promote intake of liquid in a blood channel.
Endurance to To. it is not identical at different animals even of one look. According to experimental data of school of I. R. Petrov, the painful injury, an electric trauma, elevated temperature of the environment, cooling, ionizing radiation increase sensitivity of an organism to To.
For the person loss apprx. 50% of blood is life-threatening, and loss more than 60% is absolutely deadly if there is no bystry intervention of resuscitators. The volume of the lost blood not always defines weight To., in many cases To. can be deadly and at much smaller volume of the streamed blood, especially if bleeding occurs at wound of the main vessels. At very big loss of blood, especially after its bystry expiration, death can be caused by a hypoxia of a brain if compensatory mechanisms do not manage to turn on or will be insufficient. At long decrease in the ABP there can come the irreversible state.
In hard cases at To. the development of a scattered intravascular blood coagulation caused by a combination of two factors is possible: delay of a blood-groove in capillaries and increase in content in blood of pro-coagulants. An irreversible state as a result of long To. differs on many indicators from acute To. also approaches an end-stage of shock of other origin (see. Shock ). At the same time the hemodynamics continuously worsens as a result of emergence of a vicious circle which develops as follows. At To. transport of oxygen decreases that leads to decrease in oxygen consumption by fabrics and to accumulation of an oxygen debt, as a result of a hypoxia sokratitelny function of a myocardium is weakened, minute volume falls that, in turn, even more worsens transport of oxygen. The vicious circle can arise and some other way; as a result of reduction of transport of oxygen suffers ts.n.s., function of a vasomotor center is broken, vasomotor reflexes are weakened or perverted, the last leads to a bigger pressure drop and reduction of cordial emission that leads to further disturbance of the regulating influence of a nervous system, deterioration in a hemodynamics and decrease in transport of oxygen. If the vicious circle is not broken off, then increase of disturbances can lead to death.
Pathoanatomical changes depend on speed and the size of a loss of blood. At recurrent rather small bleedings (e.g., from a uterus at a hemorrhagic metropathia, from hemorrhoidal nodes, etc.) there are changes inherent to posthemorrhagic anemia (see. Anemia ). These changes consist in the accruing dystrophy of parenchymatous bodies, the increased regeneration of red marrow, replacement by the hemopoietic elements of fat marrow of tubular bones. Proteinaceous and fatty dystrophy of hepatocytes and fatty dystrophy of myocytes of heart is characteristic; at the same time the yellowish centers of dystrophy of a myocardium alternating with less changed sites create the peculiar stripe reminding a coloring of a tiger skin (so-called tiger heart). In cells of gyrose tubules of kidneys proliferation of kernels without division of cytoplasm with formation of the multinuclear simplast inherent to hypoxemic conditions of various etiology is observed.
Pathoanatomical damages of various large arterial and venous vessels, varicose veins of a gullet, an arrosion of vessels of walls of a tubercular cavity of a lung, stomach ulcer, etc., and also hemorrhages in fabrics in a zone of the damaged vessel and mass of the streamed blood can be found at internal bleedings. At gastric bleeding in process of advance on intestines blood is exposed to digestion, turning into tar-like weight in a large intestine. Blood in vessels of a corpse in pleural and belly cavities turns partially or remains liquid in connection with disintegration of fibrinogen. At pulmonary bleeding lungs owing to a gemaspiration in the alveolar courses take a peculiar marble form because of alternation light (air) and red (filled with blood) sites of a parenchyma.
It is macroscopically possible to revenge irregularity of a krovenapolneniye of bodies: along with an anemia of integuments, muscles, kidneys the plethora of intestines, lungs, a brain is observed. The spleen is usually a little increased in sizes, flabby, plethoric, with plentiful scraping from a cut surface. Disturbance of permeability of capillaries and change in coagulant system of blood lead to widespread petekhialny hemorrhages under serous covers, in mucous membranes went. - kish. a path, under an endocardium of a left ventricle (Minakov's spot).
Microscopically widespread circulatory disturbances in system of microcirculation of internals are found. On the one hand, the phenomena of the disseminated intravascular coagulation are observed: aggregation of erythrocytes (see), formation of fibrinous and erythrocyte blood clots (see. Blood clot ) in arterioles and capillaries that sharply reduces quantity of the functioning capillaries: on the other hand, the sharp focal trichangiectasia with education erythrocyte is noted staz (see) and strengthening of a blood-groove with a focal plethora of venous collectors. Electronic microscopically swelling of cytoplasm of endothelial cells, an enlightenment of a matrix of mitochondrions, reduction of quantity of mikropinotsitozny vesicles, expansion of intercellular joints is noted that demonstrates disturbance of transport of substances through cytoplasm and about a hyperpermeability of a capillary wall. Changes in an endothelial cover are followed by education at its inner surface of conglomerates from the thrombocytes which are the cornerstone of thrombosis. Changes of cells of parenchymatous bodies correspond to that at ischemia (see) are also presented by different types of dystrophies (see. Dystrophy of cells and fabrics ). Ischemic changes of parenchymatous cells of internals arise before everything in kidneys and a liver.
A clinical picture
Clinical manifestations To. not always correspond to amount of the lost blood. At the slow expiration of blood even its considerable loss can not have clearly the expressed both objective, and subjective symptoms. Objective symptoms considerable To.: skin, pale mucous membranes, a haggard face, pale, wet with a grayish shade, the sunk-down eyes, a frequent and low pulse, decrease in arterial and venous pressure, hurried breathing, in very hard cases periodic, like Cheyn — Stokes (see. Cheyna-Stokes breath ); subjective symptoms: dizziness, weakness, blackout, dryness in a mouth, strong thirst, nausea.
To. happens acute and chronic, the varying severity compensated and noncompensated. For an outcome and treatment the amount of the lost blood, speed and duration of its expiration have great value. So, at young healthy people loss of 1,5 — 2 l of blood at the slow expiration can proceed without clinically expressed symptoms. An important role is played by the previous state: overfatigue, overcooling or overheating, an injury, the shock accompanying a disease etc. and also gender and age (women are more hardy to To., than men; are very sensitive to To. newborns, babies and elderly people).
To approximately classify weight To. it is possible on reduction of OTsK. Moderate degree — loss less than 30% of OTsK, massive — is more than 30%, deadly — it is more than 60%.
Assessment of degree of blood loss and methods of its definition — see. Bleeding .
However weight of a condition of the patient is defined first of all on a wedge, a picture.
Treatment is based on strengthening of mechanisms of compensation, to-rymi the organism, or their imitations has. The best way liquidating both a circulator, and anemic hypoxia is transfusion of compatible blood (see. Hemotransfusion ). Along with blood were widely adopted blood-substituting liquids (see) which use is based that loss of plasma and, therefore, reduction of OTsK is transferred by an organism much heavier, than loss of erythrocytes. At heavy To. before blood typing treatment should be begun with infusion of blood-substituting liquids, in necessary cases even on site injuries or during the transportation. In mild cases it is possible to be limited only to one blood-substituting liquids. Hemotransfusion or eritrotsitny weight (I eat.) it is necessary during the falling of hemoglobin lower than 8 g % and indicators of a hematocrit less than 30. At acute To. treatment is begun with jet injection and only after raising of the ABP is higher than a critical level (80 mm of mercury.) and improvements of a condition of the patient pass to drop. In cases of the raised bleeding and the hypotonias which are not giving in to correction by transfusion of stored blood direct hemotransfusion from the donor is shown, a cut gives more expressed effect even at the smaller volume of infusion.
At long decrease in the ABP hemotransfusion and blood-substituting liquids can be inefficient and shall be added with medicamentous means (cardiacs, corticosteroids, adrenocorticotropic hormone, antigipoksant) which normalize disturbances in a metabolism. Administration of heparin and fibrinolysin in hard cases and at a late initiation of treatment prevents emergence of the trombogemorragichesky syndrome developing in case of scattered intravascular coagulation (see. Hemorrhagic diathesis ). The drugs raising a vascular tone, especially pressor amines are contraindicated to a complete recovery of volume of blood. Increasing a vasospasm, they only aggravate a hypoxia.
The dose of the entered blood and blood-substituting liquids depends on a condition of the patient. Ratios of volumes of blood and blood-substituting liquids are approximately accepted the following: at a loss of blood to 1,5 l enter only plasma or blood-substituting liquids, at a loss of blood to 2,5 l — blood and blood-substituting liquids in the ratio 1:1, at a loss of blood of St. 3 l — blood and blood-substituting liquids in the ratio 3:1. As a rule, at this OTsK it has to be recovered, the indicator of a hematocrit shall be more than 30, and the maintenance of erythrocytes — apprx. 3,5 million / mkl.
the Forecast depends on the general condition of the patient, amount of the lost blood and especially on timely begun treatment. At early and vigorous treatment even very heavy To., accompanied with a loss of consciousness, heavy frustration of a respiratory rhythm, extremely low ABP, comes to an end in an absolute recovery. Recovery of vital signs is possible even at approach a wedge, death (see. Terminal states ). Worsens the forecast, but does not do it remediless development of a cross heart block, disturbance of intra ventricular conductivity, emergence of extrasystoles, an idioventricular rhythm (see. Heart block ). At timely treatment the sinoatrial rate is recovered. At treatment considerable To. after recovery of OTsK indicators of acid-base equilibrium are normalized after recovery of a hemodynamics, but contents organic to - t becomes more, than was at the end To., what is connected with their washing away from fabrics. At patients various disturbances are observed acid-base equilibrium (see) within several days after substitution heavy To., and a bad predictive sign is change of acidosis with an alkalosis with the 2nd days after its substitution. To. even moderately severe, accompanied with a scattered intravascular blood coagulation at overdue treatment, can pass into an irreversible state. The main signs of successful treatment To. normalization of systolic and especially diastolic pressure, warming and a pinkness of skin, disappearance of perspiration are.
Blood loss in the medicolegal relation
In court. - medical practice usually meet effects acute To., edges serves as the main reason for death at the injuries which were followed by massive outside or internal bleeding. In similar cases court. - medical examination establishes approach of death from acute To., existence and the nature of communication between damage and a cause of death, and also (if necessary) defines amount of the streamed blood. At survey of a corpse the picture of an acute anemia is found. Pallor of integuments pays attention, livors mortis are expressed poorly, internals and muscles are anemic, pale. Under an endocardium of a left ventricle of heart are observed characteristic of death from To. hemorrhages in the form of thin spots and strips which diagnostic value was for the first time established in 1902 by P. A. Minakov. Usually Minakov's spots of dark red color, well konturirovana, to dia. 0,5 cm and more. Are more often localized in the field of an interventricular partition, is more rare — on papillary muscles at a fibrous ring. Their pathogeny is finally not found out. P. A. Minakov connected their education with significant increase in negative diastolic pressure in a cavity of a left ventricle at massive losses of blood. Other authors explain their emergence with irritation of c. N of page under the influence of a hypoxia. Minakov's spots meet more than in half of cases at deaths door from acute To., therefore their assessment is carried out in total with other changes. In cases, when death from To. comes quickly owing to acute bleeding from large blood vessels (an aorta, a carotid artery, a femoral artery) or from heart, morfol, the picture of an acute anemia is not expressed, bodies at the same time have almost usual coloring.
In court. - medical practice the great value is given to determination of amount of the streamed blood both at internal, and at outside bleedings. At wound of large blood vessels death is possible at bystry loss apprx. 1 l of blood that it is connected not so much with the general desalination, how many with sharp falling of blood pressure and an anemization of a brain. Determination of amount of the blood which streamed at outside bleeding is made by definition of a solid residue of blood and its subsequent recalculation on liquid. The solid residue is determined or comparison of weight of sites of a spot of blood and a subject carrier, identical on the area, or by extraction of blood from a spot by alkaline solution. Recalculation of a solid residue on liquid blood is made proceeding from the fact that 1000 ml of liquid blood on average correspond to 211 g of a solid residue. This method allows to make definition only with the known accuracy rate.
At bleeding also extent of treatment of the damaged soft tissues for the solution of a question of the term of life of the victim is considered.
At expert assessment it is necessary to remember a possibility of bleeding as a result of disturbances in system of a blood coagulation (it is checked by collecting detailed anamnestic data at relatives of the dead).
Bibliography: Avdeev M. I. Forensic medical examination of a corpse, M., 1976, bibliogr.; Wagner E. A. and Tavrovsky V. M. Transfusion therapy at acute blood loss, M., 1977, bibliogr.; Veyl M. G. both Sh at and N of. Diagnosis and treatment of shock, the lane with English, M., 1971, bibliogr.; Kulagin V. K. Pathological physiology of an injury and shock, L., 1978; Pathological physiology of extreme states, under the editorship of P. D. Gorizontov and H. N. Siroti-nina, page 160, M., 1973; Petrov I. R. and Vasadze G. Sh. Irreversible changes at shock and blood loss, L., 1972, bibliogr.; G. M. nightingales and P and d-z and in and G. G's l. Blood loss and regulation of blood circulation in surgery, M., 1973, bibliogr.; Progress in surgery, ed. by M. Allgower and. lake, v. 14, Basel, 1975; San-dri tter W. a. L a s with h H. G. Pathologic aspects of schock, Meth. Achiev. exp. Path., v. 3, p. 86, 1967, bibliogr.
V. B. Koziner; H. K. Permyakov (stalemate. An.); V. V. Tomilin (court.).