[Antifibrillatory activity of propranolol in experimental myocardial infarct and its cardiodepressive and hypotensive action].

In experiments in nembutal anesthetized dogs the authors studied the dependence between the antifibrillation activity of propranolol, which was appraised according to the value of the ventricular fibrillation thresholds and the rate of spontaneous fibrillation after occlusion of the coronary artery, and the cardiodepressive and hypotensive action of this agent. It is shown that it is possible in principle to preserve the antifibrillation activity of propranolol infused intravenously in a dose of 1 mg/kg for correcting its cardiodepressive and hypotensive effect in combined intravenous infusion of 0.02 mg/kg corglycon.

[Ventricullar fibrillation in the acute stage of myocardial infarct. II. The characteristics of the heart functional changes in experimental myocardial infarct complicated by ventricullar fibrillation].

In acute experiments on dogs, occlusion of the anterior descending branch of the left coronary artery induced two-phase changes in the cardiac and stroke output (which increased at first and then decreased), drop in arterial pressure, and decrease in the rate of cardiac contractions. The experiments which terminated in ventricular fibrillation were characterized by a number of peculiarities: a more rapid replacement of the phase of primary increase in the cardiac and stroke output by the phase of their decrease; a sharper drop in arterial pressure as compared with that in experiments without fibrillation; marked decrease in cardiac activity which in experiments without fibrillation underwent two-phase changes, it increased a little at first and then decreased.

[Ventricular fibrillation in acute phase of myocardial infarct. 1. Relationship between the development of ventricular fibrillation in myocardial infarct and previous rhythm disorders].

The author analyses the results of experimental studies in dogs and cats, that included a continuous recording of ECG, electrogram and monophase cardiac potentials during 1 hour following coronary artery ligation. The ligation caused bradycardia, but no correlation was found between the degree of bradycardia and the development of extrasystole and ventricular fibrillation. Extrasystole developed in 100% of the experiments in which the coronary artery ligation resulted in ventricular fibrillation, and in 66% and 87% of those without this complication, conducted in dogs and cats respectively.