[Appraisal of the status of metabolism in myocardial layers in acute left-ventricular insufficiency using data from radionuclide examination methods].

Experiments were conducted on 35 mongrel dogs. It was demonstrated in series I experiments that exclusion of a 14.5% myocardial area from the heart mass induces acute left-ventricular insufficiency manifested by authentic decrease of the cardiac ejection and left-ventricular output index and a 22% increase of pressure in the left atrium and pulmonary artery. The left-ventricular coronary blood flow and the blood flow in the myocardial layers of the right and left ventricles and in the interventricular septum increased significantly as compared to the control values. Distal to the area of the necrosis, however, the layer-by-layer flow of the blood in the left ventricle had a marked tendency to increase. In series II experiments, in myocardial necrosis the volume load, which was equal to one half and one initial circulation volume, mobilized the heart contractile activity, which led to increase of the coronary blood flow which was less than the initial level in series I experiments. Analysis of layer-by-layer blood flow after a volume load equal to one initial circulation volume showed it to be markedly increased in all layers of the left-ventricular anterior wall above and below the necrotic area, in the left-ventricular posterior wall, in the interventricular septum, and in the right-ventricular anterior wall. The increase of 201Tl-chloride accumulation in the myocardial layers under the studied conditions is evidently linked with activation of metabolic processes responsible for increase of heart contractile activity and, consequently, for increased uptake of 201Tl from circulation by the intact cardiomyocytes rather than with change in redistribution of the blood flow and its increase.