Inhibition of endo- and epicardial glycogenolysis by propranolol in ischemic hearts.
The effect of coronary artery ligation on myocardial glyocogenolysis was studied in the endo- and epicardial layers of the left ventricle in dogs pretreated with saline or 1 mg/kg of propranolol. Coronary artery ligation was performed by ligating one of the small branches of the left anterior descending coronary artery. Even after coronary artery ligation, neither increase in phosphorylase activity nor breakdown of glycogen was observed in both layers of ischemic region of myocardium in propranolol-pretreated dogs. These results indicate that pretreatment with propranolol inhibits the increase in glycogenolysis being caused by coronary artery ligation. Propranolol howefer, did not inhibit completely the coronary artery ligation-induced increase in glucose 6-phosphate and lactate and decrease in phosphocreatine in the myocardium, especially in the endocardial layers.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003327:Coronary Disease / Q000378:metabolism*; D003331:Coronary Vessels; D004285:Dogs; D004699:Endocardium / Q000378:metabolism; D005260:Female; D005958:Glucosephosphates / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism*; D007773:Lactates / Q000378:metabolism; D008026:Ligation; D008297:Male; D009206:Myocardium / Q000378:metabolism; D010496:Pericardium / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism; D006005:Phosphorylases / Q000378:metabolism; D011433:Propranolol / Q000494:pharmacology*
D005958:Glucosephosphates; D007773:Lactates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D006003:Glycogen; D011433:Propranolol; D006005:Phosphorylases