ABSTRACT
The experiments on anaesthetized dogs have shown that with artificial ventilation and open chest adrenalin in arrhythmogenic and nonarrythmogenic doses enhances glycogenolysis in the heart proportionally to the dose used Block of beta-adrenergic receptors by propranolol decreased the activation of glycogenolysis in the ischaemic zone and the frequency of ventricular fibrillation after occlusion of the coronary artery. Exhaustion of noradrenaline reserves by reserpin does not influence the intensity of glycogenolysis and the frequency of fibrillation in the acute period of myocardial infarction. It is believed that the activation of glycogenolysis in experimental myocardial infarction is related to the action of adrenalin.
Subject(s)
Epinephrine/physiology , Glycogen/metabolism , Myocardial Infarction/chemically induced , Myocardial Infarction/complications , Norepinephrine/physiology , Ventricular Fibrillation/chemically induced , Animals , Arrhythmias, Cardiac/metabolism , Dogs , Male , Myocardial Infarction/metabolism , Myocardium/metabolism , Propranolol/pharmacology , Receptors, Adrenergic, beta/drug effects , Reserpine/pharmacology , Ventricular Fibrillation/metabolismABSTRACT
The first minutes of coronary artery occlusion in dogs showed the enhancement of glycogenolysis which was provided by the activation of phosphorylase, phosphofructokinase, triosophosphate isomerase and lactate dehydrogenase. The aldolase and glyceroaldehyde-3-phosphate dehydrogenase reactions were the rate limiting steps. The activation of glycogenolysis seems to be the result of a combined action of hypoxia and catecholamines.