Abstract Using the blood-bathed technique of Vane we induced acute coronary occlusion in the dog and subsequently detected adrenaline release into the circulatory system, determined the rate of release and documented its significance for induction of cardiac arrhythmias. In the intact anesthetized dog, adrenaline excess of the magnitude released after coronary occlusion was sufficient to injure the healthy myocardium and to induce unfavorable metabolic systemic alterations. Subsequently, clinical research has documented that a serious clinical course of acute myocardial infarction is associated not only with enhanced excretion of catecholamines but also with augmentation of plasma renin activity and aldosterone levels. The positive therapeutic effect of aldosterone antagonists in acute myocardial infarction has been documented. The clinical value of our results, which were obtained in experimental and clinical studies, was later confirmed in multi-center trials.