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Biomedical subjects

N N Beskrovnova

Publications and source records attributed to N N Beskrovnova.

At least 19 recordsLinked to original sources
PubMed1992

[Mechanisms of arrhythmias and heart fibrillation in myocardial ischemia and the possible role of Purkinje cells in their origin].

Morphological, metabolic and functional features of the heart subendocardial areas under normal conditions and at early periods of myocardial ischemia are considered in this review. It is suggested that the arrhythmias and fibrillation developing at early stages of ischemia arise in the subendocardium. The initiators of this process may be altered Purkinje's cells as precisely these cells in ischemia acquire certain characteristics necessary for the development of ectopic foci, namely: cells remaining viable should have a lowered threshold of excitability and a capacity for automatism. Further study of Purkinje's cells is particularly important for understanding of causes and prevention of a high lethality at acute phase of the myocardial infarction.

Arrhythmias, Cardiac↗
PubMed1991

[Alterations of the aortic endothelium ultrastructure after the administration of cholesterol oxidation products to rabbits].

Intravenous administration of 7 alpha-hydroxycholesterol and cholestane-triol at the dose of 2.5 mg/kg produces, one day later, ultrastructural alteration of aortic endothelial cells such as cytoplasmic vacuolation, protruding and crateriform surface defects, subendothelial oedema with a subsequent exfoliation of endotheliocytes. The endothelial damage was more pronounced after the administration of equal doses of cholestane-triol as compared to 7 alpha-hydroxycholesterol. Ultrastructural changes 10 days after oral administration of 500 mg/kg cholesterol mixed with its auto-oxidation products were similar to those developing after cholestane-triol and 7 alpha-hydroxycholesterol. Cholesterol free of the oxidation products at the same doses did not produce alterations in the rabbit aortic endothelium.

Animals↗
PubMed1989

Ultrastructure of Purkinje cells in the subendocardium and false tendons in early experimental myocardial infarction complicated by fibrillation in the dog.

The effect of regional myocardial ischemia complicated by ventricular fibrillation (VF) on the ultrastructure of subendocardial (SE) and false tendon (FT) Purkinje cells (PC) was studied in anesthetized dogs. In all cases of early ischemia with spontaneous VF, many PC exhibited ultrastructural damage as early as 2 min after the onset of ischemia. The changes noted were: intercalated disk dissociation, sarcoplasmic reticulum vacuolization (SRV), supercontraction, mitochondrial swelling, and sarcolemmal defects (rigor cells). The appearance of at least some rigor PC seemed to precede spontaneous VF, since these cells were absent from the conduction systems in control hearts in which VF was induced by electric shock or reperfusion, from hearts from sham-operated dogs, or from hearts subjected to longer periods of uncomplicated myocardial infarction. These observations indicate that alterations in SE and FTPC may play a role in the pathogenesis of sudden death due to early myocardial ischemia. The mechanism of this rapid damage of PC remains obscure.

Animals↗
PubMed1989

[The role of free radical inhibitors of lipid peroxidation in protecting the myocardium from ischemic damage].

The natural antioxidant beta-carotene which, unlike phenol antioxidants such as dibunol and SPN-6, is capable of exhibiting antioxidative properties under low partial oxygen pressure (ischemia), has been found to increase the activity of antioxidative enzymes in the intact and infarct myocardium and to greatly exert a more antinecrotic action when given orally in a dose of 20 mg/kg in models of rat coronary-occlusion myocardial infarction than the phenol antioxidants mentioned above. Intravenous administration of copper-containing enzymes utilizing O2 superoxide dismutase (SOD), 4 mg/kg, or ceruloplasmin, 50 mg/kg, as with a highly disperse copper powder promoting a substantial increase in antioxidative enzyme activity in the rat myocardium has been demonstrated to reduce the zone of myocardial ischemic lesion in rats and to largely enhance postoperative survival rates in the animals. Three hours following intravenous SOD, an electron microscopic examination of rat ischemic myocardium showed a considerable fall in the structural and functional damages to cardiomyocytes in the periischemic area. The findings suggest that free radical processes make a contribution to ischemic cardiomyocyte lesion and open the way for pharmacological therapy of postischemic abnormalities with enzymatic and non-enzymatic preparations of antioxidants.

Animals↗
PubMed1987

Normalization of the stress-induced cardiac rhythm disturbances by activation of the positive emotiogenic area of the lateral hypothalamus in the rabbit.

Results of experiments indicated, that activation of the positive emotiogenic areas of the lateral hypothalamus abolished what may be considered emotionally induced cardiovascular disturbances. The by immobilization and hypothalamic defence area stimulation provoked increase of blood pressure and heart rate returned to control values, the giant T waves of ECG and dysrhythmias if present disappeared. The morphological abnormalities in the subcellular structures of the myocardium due to prolonged stress stimulation, could not be annulled by the evoked positive emotions. On the other hand the activation of the positive emotiogenic area of the hypothalamus preceded and overlapped with that of the defence area and immobilization, it prevented the functional as well as morphological cardiovascular changes.

Animals↗
PubMed1987

[Parasympathetic regulation of cardiac rhythm in delta sleep-inducing peptide deficiency].

The effect of delta-sleep peptide (DSP) deficiency on the parasympathetic regulation of the heart rate was studied on 35 rabbits. It was established that the injection of an-serum (titer-1:2000-1:3000) leads to the attenuation of parasympathetic influences: heart rate increase in freely behaving animals and a decrease in negative chronotropic effect with direct vagus irritation. Antiserum, like DSP, administration causes practically no damage of the myocardial ultrastructure.

Animals↗
PubMed1986

[Mechanisms of the development of the terminal state in experimental emotional stress].

The development of ventricular fibrillation associated with experimental emotional stress was studied in chronic rabbit experiments. Changes in myocardial-fibre action potentials, thresholds for ventricular fibrillation and its precursors, blood and myocardial catecholamine levels and heart-muscle ultrastructure were examined. Emotional stress was shown to increase, via sympathoadrenal activation, functional and structural heterogeneity of the myocardium, leading, alongside other causes, to arrhythmias and death from ventricular fibrillation. Moderately prevailing parasympathetic effects on the heart during stress exposure contribute to the elevation of fibrillation and fibrillation precursor thresholds and prevent catecholamine rise and myocardial structural damage.

Action Potentials↗
PubMed1986

[Ultrastructure of the Purkinje cells in the subendocardium and pseudo-tendons of the left ventricle in dogs with experimental infarct complicated by fibrillation].

Ultrastructural changes of Purkinje cells located on the periphery of the cardiac conductive system (subendocardium and false tendons) were studied in dogs in the presence of ventricular fibrillation developed in 30 minutes after coronary artery ligation. Ventricular fibrillation at the early stages of experimental myocardial infarction was invariably associated with the development of multiple ultrastructural lesions in the conductive Purkinje cells of subendocardium and false tendons. These changes are without any doubt important for the pathogenesis of ventricular fibrillation in myocardial infarction and they possibly take place in cases of sudden cardiac death.

Animals↗
PubMed1985

[Changes in the ultrastructure of the myocardium after fibrillation and in the process of autolysis].

Ultrastructure of the myocardium in the experiment was studied just after the heart ventricular fibrillation and 3 h after the animal death; the results were compared to those obtained by studying ultrastructure of human myocardium in patients dying from myocardial infarction complicated by ventricular fibrillation. The similarity of ultrastructural and autolytic changes was revealed in both series of observation. Overcontraction of myofibrils and redistribution of the mitochondria in cardiomyocytes, increase of the sarcoplasmic reticulum vesiculation, oedema of sarcoplasm, structural alterations of intercalative discs, later appearance of the symptoms of the irreversibility of lesions in the mitochondria and early penetration of colloidal lanthanum particles in rigor cells may serve ultrastructural diagnostic symptom of ventricular fibrillation. A better preservation of Purkinje's cells as compared to the contractile cardiomyocytes is also demonstrated.

Animals↗
PubMed1984

Pacemaker automatism activity in atrioventricular valves and its possible role in producing cardiac arrhythmias.

In the atrioventricular valves of the hearts of 161 rabbits the authors found permanent spontaneous automatism activity. Isolated leaflets of these valves were examined with the aim to detect the electrophysiological and morphological characteristics of pacemaker formations constituting the substrate of spontaneous automatism. It was found that these formations consist of pacemaker cells of three types: P-cells, cells of intermediary type and Purkinje-type cells. Further, it was found that a decisive role in the genesis of spontaneous excitations of pacemaker cells of AV valves is played by the slow Na-Ca channel. Examination documented good innervation of the pacemaker formations, and the specific effect of mediators [acetylcholine, adrenaline, noradrenaline] on their automatism was investigated. Investigations on isolated rabbit hearts evidenced that impulses originating from the heterotopic excitation focus, localized in the AV valve leaflets, can be conducted into other compartments of the heart and can cause cardiac arrhythmias.

Acetylcholine↗
PubMed1981

[Effect of reserpine on the ultrastructure and electrical instability of the heart].

The time course of ultrastructural and electrophysiological disorders and their role in sudden death of ventricular fibrillation at various intervals of desympathization caused by reserpine administration were studied. Early in the effect of reserpine (up to 30 min), glycogen granules were found to accumulate in the sarcoplasm of cardiomyocytes. At later intervals (1-24 hours), along with glycogen accumulation destructive lesions of organoids were observed in the form of myofibrillar recontraction, destruction of mitochondria, degeneration of sarcolemma. These changes are morphologic reflections of metabolic disorders developing in the myocardium under conditions of acute desympathization of the patient, and may be one of the causes of increased vulnerability of the heart in fibrillation.

Animals↗
PubMed1980

[Possibility of determination of the type of cardiomyocyte death with the aid of ultrastructural analysis].

An attempt was made to determine the ultrastructure of those types of cell death which may occur experimentally only during life and to compare them with the findings obtained from the autopsy materials of the myocardium of persons dying suddenly or from acute myocardial infarction. Three ultrastructural types of cellular death were determined in the experimental and autopsy material: primary-ischemic, primary-calcium, and secondary-calcium types. The ultrastructural pattern of some irreversible changes found in the autopsy material may be used for retrospective judgement on the mechanisms of cell death. The results obtained do not completely solve the problem of interpretation of ultrastructural findings in examinations of human postmortem materials although open some approaches for using electron microscopy in addition to the main sources of information in the study of sudden death.

Acute Disease↗
PubMed1979

[State of microcirculation in various zones of the heart in myocardial infarct complicated by congestive circulatory insufficiency].

A definite correlative connection has been revealed between the clinical course of myocardial infarction, the extent of affection of the heart muscle, the severity of the atherosclerotic process in the coronary arteries, and the condition of microcirculation in different zones of the heart. The severest affections of the heart muscle, stenosing coronarosclerosis and disorders of microcirculation in different zones of the heart were encountered in patients with myocardial infarction marked by a recurrent course and complicated by cardiogenic shock or congestive circulatory insufficiency. It is shown that the character of changes in microcirculation determines to a great measure the later condition of the structure and function of the myocardial muscle cell in areas near and remote from the infarction.

Adult↗
PubMed1979

[State of the myocardial contractile structures in different areas of the heart in myocardial infarct complicated by cardiogenic shock and congestive circulatory failure].

In myocardial infarction, destructive changes develop in the contractile elements of the heart muscle in the peri-infarction zones. The degree and extent of the myofibril involvement depend on the clinical course of myocardial infarction, the drug therapy applied, and the distance from the focus of necrosis. The most marked destructive changes were in the prenecrotic zone of the myocardium in individuals with cardiogenic shock or severe congestive cardiac failure with clinical symptoms of glycoside intoxication. Gross focal contractures of myofibrils were found, which subsequently underwent fibrinoid necrosis. There were also areas of myofibril relaxation with dissociation of the actin fibers and destruction of the z-disks. The destructive changes in the myofibrils are due to a great extent to the effect of catecholamines, myocardial hypoxia, and glycoside intoxication. The disturbed orientation of the myofibril bundles in patients with recurrent myocardial infarction may play an essential role in the decrease of the myocardial contractile function and the development of extrasystolic arrhythmias.

Aged↗