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Biomedical subjects

S V Shormanov

Publications and source records attributed to S V Shormanov.

At least 19 recordsLinked to original sources
PubMed1991

[Arterial bed of myocardium in congenital heart defects].

Structural reconstruction of the myocardial arteries seen in congenital heart disease was analyzed and its importance for cardiac activity was defined on the basis of studying case reports, postmortem examinations and morphological data on 127 abnormally formed hearts. It has been established that developmental abnormalities of the heart may be accompanied by myocardial hypertrophy and lesions of the coronary arteries, having an adaptation and pathological character. The former ones lie in hypertrophy and hyperplasia of vascular wall muscles, whereas the latter ones in sclerosis and thrombosis of the arteries, thus creating prerequisites for heart decompensation.

Cadaver↗
PubMed1990

[Adaptive structures of the venous bed of the heart in normal state and in congenital defects].

By means of a complex of anatomical, morphometrical and histological methods in 45 normally formed and in 179 abnormally developed hearts from persons of both sex died at various age, various links of the venous blood outflow from the myocardium have been investigated. Various parts, differing in a number of morphological signs, have been distinguished: coronary sinus, subepicardial veins, paired sinusoid veins, sinusoids of the myocardium and endocardial eversions. Regulation of their blood stream is performed by a system of simple muscular and infundibular valves, by intimal and muscular cushions, by connective tissue and muscular bridges. These adaptive structures occur in the normal heart also, but at congenital heart diseases, however, they reach an essentially greater development. Their localization is predominantly in the area of venular, vein, sinusoid bifurcations and endocardial eversions. Regular functioning of some parts of them is performed not by nonstriated, but by the cardiac muscular tissue. The coordinating work of the formation in question is one of the factors, that ensures the state of compensation in the defectively formed heart.

Adaptation, Physiological↗
PubMed1989

[Morphologic changes of the coronary vessels in patients with congenital heart defects].

Results of the study of the structural changes in the coronary vessels at various levels of ramification in patients with heart defects are presented and their role in the heart compensation and decompensation is shown. 127 hearts with congenital defects and 45 control children's hearts were studied. It is established, by means of anatomical, histologic and morphometric methods, that the heart defects are followed by the hypertrophy of the heart regions involved functionally, this being combined with an adaptive and pathologic rearrangement of coronary arteries and veins. The former is expressed in the vessels hyperplasia, thickening of their wall, and in the appearance in the vascular wall of oblique and longitudinal smooth myocytes (this is of importance for the maintenance of the heart compensation state). The latter is manifested in sclerosis, sometimes also thrombosis of the coronary arteries and veins this creating the basis for the heart failure.

Cardiomegaly↗
PubMed1989

[Adaptive structure or arterial and venous sections of the coronary basin in congenital defects of the heart].

A complex of histological techniques was used to examine 179 abnormally developed hearts. The vascular bed of the organ showed a number of adaptive structures that controlled blood motion. In the arterial portion, they appeared as advential and intimal musculature, polypoid cushions, muscular constrictors, and precapillary sphincters; in the venous one, they involve the system of simple and muscular valves, intimal and muscular cushions, connective tissue and muscular bridges. All these structures were found to be located in the area of cardiac vascular bifurcations. The regulatory function of some of the structures is effected by cardiac musculature rather than smooth muscles. The coordination of these formations provides the prolonged maintained compensatory status of the deformed heart. The abnormal changes in the adaptive structures of coronary system amount to their dystrophy, atrophy, and sclerosis, which is one of the manifestations of cardiac decompensation.

Adaptation, Physiological↗
PubMed1988

Comparative analysis of structural change in a free autovenous graft and in a transplant with spiral reinforcement after correction of experimental arterial defects.

In sixty-four dogs, a comparative analysis was made of structural changes produced in the wall of free autovenous graft and of a transplant strengthened by a spiral reinforcement (lavsan monothread) after transplantation of femoral vein segments into the common carotid artery. Histological and morphometric examinations made in an interval ranging from 3 days to 1 1/2 years after surgery showed that the strengthening of the venous graft by means of a reinforcement prevents its overextension when functioning as an artery, and keeps the endothelium intact. This reduces the danger of thrombotic complications in the operation area. The spiral reinforcement at the same time prevents compression of the vein by surrounding cicatricial tissue as well as an aneurysmatic extension of the transplant.

Animals↗
PubMed1987

[Changes in the walls of autologous venous grafts after transplantation into arteries].

In 54 dogs 76 operations on plastics of the common carotid arteries with the femoral vein segments have been performed. The animals have been observed for 3 days--1.5 years. The grafts, preserving their permeability, have been studied using a complex of anatomical, histological and micromorphometric techniques. At early stages after the operation (up to 7 days), dystrophic and necrobiotic changes predominate in the wall of the venous graft. As a result of overstretching of the denervated and devascularized vessel, under the effect of a high arterial pressure, nearly total rejection of the endothelial lining takes place, as well as death of some smooth myocytes in the middle tunic; this determines appearance of early thromboses. During 2-6 months after the operation, against the background of a good revascularization of the graft, restorative and adaptive changes develop in its wall. The intima becomes thick at the expense of formation of the obliquely situating layer of myocytes, as well as the result of parietal thromboses organizing on the deendothelized internal surface. These thickenings are especially well seen in the zones of anastomoses. In 6 months--1.5 years after the transplantation into the artery, as a result of constriction of the vessels feeding the graft and reduction of blood stream along them, atrophic and sclerotic changes increase in the wall. The intimal thickenings often acquire the pattern of fibrous patches, that make the lumen more narrow; this can cause appearance of late occlusions and thromboses of the grafts.

Animals↗
PubMed1985

[Adaptive structures of the arteries of the heart participating in the regulation of coronary circulation].

By means of a complex of anatomical, histological and histochemical methods cardiac vessels have been studied in 20 control dogs and in 84 dogs with experimentally produced circulatory disturbances peculiar for congenital heart diseases presented as an open arterial duct, coarctation of the aorta and the pulmonary trunk stenosis. The experimental animals have been observed for 6-12 months. In the animals with experimentally produced disturbances of the general and coronary hemodynamics hyperplasy in the coronary branches of the arteries appears, it is more pronounced in functionally loaded cardiac parts, as well as thickening of their walls at the expense of new formations and hyperthrophy of smooth muscle cells. In both control and experimental dogs in the coronary vessels at various branching levels certain formations are revealed; they are of compensatory-adaptive value: intimal and adventitial musculature, polypoid pulvinars, muscular-elastic constrictors, muscular cuffs and precapillary sphincters. They differ in structure, sources of their origin and in their functional value. Degree of their manifestation increases significantly after reproduction of the hemodynamic disturbances in the heart vascular system. The active role of these formations in regulation of the coronary circulation is demonstrated owing to a high content of ribonucleinic acid and glycogene in their smooth muscle cells and also an elevated succinate dehydrogenase, cytochromoxydase, acid and alcaline phosphatase activities.

Animals↗
PubMed1985

[Outflow pathways of venous blood from the myocardium in the dog and structures participating in their regulation].

The intramural pathways of the venous blood outflow from the cardiac wall have been studied histologically, histochemically and micrometrically in 20 control and 84 experimental dogs with an artificially produced circulatory disturbances, peculiar for congenital heart disease (open arterial canal, coarctation of the aorta and stenosis of the pulmonary trunk). The experimental animals have been observed for 6-12 months. In the venous line of the coronary basin several morphologically differed parts, anatomically and functionally connected between themselves and ensuring blood outflow from the myocardium, are distinguished: coronary sinus, subepicardial veins, paired sinusoid veins, myocardial sinusoids and endocardial cushions. In each of them there are their own adaptive structures, participating in regulation of the venous blood stream. In the cardial sinus, in the subepicardial and paired sinusoid veins--these are valves of various complexity. In the myocardial sinusoids, the regulatory function, together with the valves, are performed by the intimal and muscle cushions, connective tissue and muscle bridges. In the endocardial cushions they are realized by the valves, muscle sphincters, bundles of obliquely and longitudinally oriented leiomyocytes. All the adaptive structures mentioned are also found in the hearts of the control animals. Under modelling various hemodynamic disturbances, the degree of their development increases sharply. The latter ensures the maintenance of an optimal regimen of blood circulation in the myocardium of a functionally loaded heart and prevents development of decompensation in the organ.

Adaptation, Physiological↗
PubMed1983

Morphological changes of the heart arteries in experimental stenosis of the pulmonary artery trunk and their reversibility after correction of the defect.

Experimental stenosis of the pulmonary artery trunk was induced in 48 puppies, and using a comprehensive histomicrometric method the condition of the heart arteries was investigated during the defect and after its correction. Six to twelve months after the operation, the young dogs developed cardiac hypertrophy, hyperplasia of the minute branches of the coronary arteries and hypertrophic-hyperplastic changes in the wall of the coronary arteries at all levels of their branching. In 18 puppies, the stenosis was corrected, which after 6 to 12 months led to a regression of the hypertrophic changes in the heart and its vessels. At the same time, the arterial bed got gradually adapted to the new conditions of circulation, which was manifested by the fact that part of the minute arteries changed into closing-type arteries, and blood flow in them decreased.

Animals↗
PubMed1982

[Morphologic changes in the coronary arteries in experimental coarctation of the aorta and following its correction].

In 33 puppies 2-4 months of age the model of a congenital heart disease was made as coarctation of the aorta. In 6-12 months 18 animals were taken to study, and in 15 animals the coarctation was removed. The latter animals were observed for other 6-12 months. The hearts of both groups were separately weighed, and the vessels of the coronary system were studied by means of a complex of histological and morphometric methods. Simultaneously, the number of smooth muscle cells, as well as the area and volume of their nuclei in media of small coronary arteries were estimated. At the experimental coarctation of the aorta certain hypertrophic-hyperplastic changes in coronary arteries at all branching levels take place. They are of a compensatory-adaptive character and reflect certain reactions of the vascular wall to an increased coronary hemodynamics under conditions of hyperfunction and hypertrophy of the cardiac muscle. Surgical removal of the coarctation is accompanied with a reduce of the hemodynamic loading of the heart, diminished degree of hypertrophy of the organ and a marked decrease of the hypertrophic-hyperplastic changes in its vessels. At the same time, the cardiac vascular system is adapting to the new conditions of circulation: rearrangement of some coronary arteries and arterioles according to the closed type and reduction of circulation in the vascular branches which have lost their importance in feeding the myocardium.

Animals↗
PubMed1980

[Structural changes in cardiac vessels in experimental patent ductus arteriosus].

In 43 puppies an experimental arterial duct was produced. The animals were observed for 1--2 months and then killed. Their hearts were separately weighed, and their vessels were studied by means of a complex histomicrometry method. In the puppies with the artificially produced arterial duct, hypertrophy of both cardiac ventricles was gradually developing, combined with thickening medial tunica of the coronary arteries at all levels of their branching. Simultaneously, the oblique-longitudinal musculature of the vascular walls grew stronger. In the distributing arteries it occurred at the expense of the muscular fasciculi situated in adventitia, in the resistance arteries--at the expense of the fasciculi situated in intima. The hypertrophic-hyperplastic changes noted in the vessels of the coronary system were connected with cardiac hypertrophy and with disorders of coronary hemodynamics.

Animals↗
PubMed1979

Structural rebuilding of pulmonary vessels at various haemodynamic shifts in the lesser circulation.

The rebuilding of pulmonary vessels at hypo- and hypertension in the lesser circulation was studied in 41 puppy dogs, in which hypotension had been induced by stenosing the pulmonary artery. Eighteen animals were successively sacrificed 6--9 months after the surgery. Histological examinations revealed atrophic and sclerotic lesions of the pulmonary arteries. In the remaining 23 animals, various anastomoses were formed between the systemic and pulmonary circulation systems, which led to the formation of hypertrophic and hyperplastic alterations in the pulmonary vessels and to pulmonary hypertension.

Animals↗
PubMed1979

[Pathologic diagnosis of certain congenital heart defects].

Morphometrical examinations of 265 normally formed hearts collected at autopsies of infants under 2 years of age were used as a control of the heart weight and size of the pulmonary trunk and aorta. The time of anatomical closing of the arterial duct and oval window were established. Comparisons of the results of morphometry of normal and 173 malformed hearts with the tabulated data were used to develop objective criteria for pathological diagnosis of congenital heart diseases: open arterial duct and centrally located defect of the interatrial septum in infants dying within the first two months of life. The criteria for the detection of marginal forms of stenosis of the pulmonary trunk ostium and isolated coarctation of the aortal isthmus were established.

Age Factors↗
PubMed1978

[Structural changes in the vessels of the heart in different hemodynamic disorders in the coronary basin].

Coarctation of the aorta was created in 15 and stenosis of the pulmonary arteri in 20 puppies. In the first experimental defect the blood inflow into the coronary basin increased, in the second the outflow from it was disturbed. The proposed method of complex histomicrometria was used to study changes in coronary vessels of various calibers. In both disorders of the coronary hemodynamics, hypertrophy of tunica media of arteries of all levels, an increase in their walls of the amount and power of obliquelongitudinal muscles, and hypertrophy of muscle-elastic sphincters in the openings of side branches going from small arteries were observed. Signs distinguishing one defect from the other were found at different levels of the vascular system of the heart. Their emergence is associated with hypertrophy of one or another part of the heart and features of the coronary hemodynamics inherent in each defect.

Animals↗