Cardioprotective effects of superoxide dismutase following coronary artery occlusion in the rat.
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Biomedical subjects
Publications and source records attributed to M M Povzhitkov.
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In the course of experimental cardiogenic shock in dogs it was found that in comparison with marked disturbances of heart function and haemodynamics in the systemic circulation, the changes in the right ventricular contractility were less conspicuous. The pulmonary arterial pressure kept at a level approaching the initial one. The pulmonary vascular resistance substantially rose at the same time, especially so in the arterioles. The left heart filling pressure did not increase. The authors assume that the changes in the pulmonary vascular resistance result from direct neurohumoral control of vascular resistance, and discuss possible mechanism of this control.
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Reaction of the capacitance vessels of the abdominal cavity and the pelvis was studied in dogs with the cardiotoxic myocardial necrosis complicated by the cardiogenic shock. The deposit of a significant volume of the circulating blood in the venous part of the vascular reservoir of the abdominal cavity and the pelvis was observed in the course of the first minutes of acute myocardial necrosis. A substantial role of reduction of the venous return to the heart in the pathogenesis of the hemodynamic disturbances accompanying the development of the cardiogenic shock is emphasized.
In tests set up on dogs under morphine-chloralose anesthesia features specific for upset cardio- and hemodynamics following a primary and repeated (against the background of a preliminarily provoked myocardial infarction) acute disruption of the coronary circulation were investigated. The development of an acute ischemia of the myocardium in animals with preliminarily induced chronic disruption of the coronary circulation was shown to be attended by more intensive than in healthy dogs hemodynamic shifts and functional disorders of the heart, whereas the reflex component of the reaction, the vasodilating reactions of the peripheral vessels, in particular, proved much less marked. Possible mechanisms accounting for differences in the derangement of the cardio- and hemodynamics in primary and repeated ischemia of the myocardium are discussed.
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