[Role of changes in myocardiocytes in the development of acute heart failure in experimental myocardial infarct].

Some problems of the pathogenesis of the development of acute cardial insufficiency were studied on the material of 2-hour experimental myocardial infarction in dogs. Acute cardial insufficiency developed owing to additional load on the heart (partial stricture of the aorta) after ligation of the posterior circumflex branch of the coronary artery. It was found that 24 hours after the removal of the immediate causes of acute cardiac insufficiency (removal of clamps from the coronary artery and aorta) the symptoms of the contractile weakness of the left heart correlated directly with electron microscopic signs of increased degeneration of intracellular structures and did not depend on the level of energetic processes in cardiomyocytes and the structure and function of sarcolemma. The restoration of the bloodflow in the previously ligated coronary artery for 2 hours did not improve the condition of the cells in the ischemic zone but enhanced reparative processes in the non-ischemized zone of the left ventricle.