[Role of glycogenolysis inhibition in the etiology of arrhythmias in coronary disease].
Under conditions of acute ischemia spontaneous fibrillation which developed in heart ventricles as well as arrhythmias which were medicamentally provoked both were accompanied by a decrease in activity of glycogen phosphorylase a. At the same time, there was a distinct increase of non-phosphorylated isoenzyme ratio to the total phosphorylase activity of the tissue and the total glycogen pool was decreased. The decrease in activity of glycogen phosphorylase a, after pharmacological correction of metabolism of highly ischemized myocardium using obzidan and digoxin at therapeutic doses, occurred simultaneously with a decrease in the level of phosphorylase b activity in the tissue. A hypothesis, considering an increase in glycogenolysis as a trigger mechanism in development of ventricle fibrillation under conditions of acute coronary occlusion, is criticized.
D000818:Animals; D003327:Coronary Disease / Q000150:complications / Q000378:metabolism*; D004077:Digoxin / Q000494:pharmacology; D004285:Dogs; D005260:Female; D006003:Glycogen / Q000378:metabolism*; D006019:Glycolysis; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D006005:Phosphorylases / Q000378:metabolism; D011433:Propranolol / Q000494:pharmacology; D014693:Ventricular Fibrillation / Q000209:etiology / Q000378:metabolism*
D004077:Digoxin; D006003:Glycogen; D011433:Propranolol; D006005:Phosphorylases
Rol'ugneteniia glikogenoliza v proiskhozhdenii aritmiĭ koronarogenno porazhennogo serdtsa.