[Role of adrenaline in the changes of ion and energy metabolism in the cardiac mitochondria in experimental myocardial infarct].

The changes in the content of K+ ions, in the respiration and oxidative phosphorylation were studied in the mytochondria of canine hearts 5 and 30 min following the ligation of the left descending coronary artery. The gradual changes in the content of intramytochondrial K+ in the mytochondria of the ischaemic zone is attributed to the decreasing rate of phosphorylating respiration and dissociation of respiration and phosphorylation. Similar, but less distinct changes were noted in the mytochondria of the non-ischaemic zone. In cases resulting in ventricular fibrillation a higher dispersion of the metabolic indices was noted: decrease in K+ content, respiration and oxidative phosphorylation in the mytochondria of the ischaemic zone is nore distinct, while in the mytochondria of the non-ischaemic zone it did not differ from what is observed in a favourable course of an experimentally induced myocardial infarction. Propranolol, given in a dose of 1 mg/kg, under normal conditions decreased the respiration rate in the mytochondria and at the same time reduced the activity of succinatecytochromium-C-oxydoreductase, producing no effect on the conjugation of respiration and phosphorylation. In case of myocardial infarction Propranolol prevented the decrease of K+ and dissociation of respiration and phosphorylation. The changes in the ion and energy exchange in the cardiac mytochondria during the acute phase of myocardial infarction are attributed to the activation of the sympathoadrenal system.