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Inhibition of endo- and epicardial glycogenolysis by propranolol in ischemic hearts

Inhibition of endo- and epicardial glycogenolysis by propranolol in ischemic hearts IN THE PREVIOUS PAPER (7) we have demonstrated in open-chest dogs that coronary artery elevated the phosphorylase activity and accelerated the breakdown of glycogen in the region of left ventricular wall that had been perfused by the ligated coronary artery, and we have also reported that the coronary artery -induced acceleration in metabolism in the endocardial layers was more rapid and marked than that in the epicardial. The mechanisms by which coronary artery produces acceleration of myocardial glycogenolysis, however, are not fully elucidated. Several investigators (5, 8, 18) have suggested that catecholamine release occurs in response to ischemia in the myocardium. If catecholamine release occurs after coronary artery in the region of myocardium that has been perfused by the coronary artery, it is possible to assume that the coronary artery -induced acceleration of phosphorylase activity and breakdown of glycogen in the dog myocardium would be inhibited by pretreatment of the dog with a beta-adrenergic blocking agent. The present study, therefore, was undertaken to examine the above assumption using propranolol as a beta-adrenergic blocking agent. MATERIALS AND METHODS Animal preparation. Mongrel dogs of either sex weighing 7-15 kg were anesthetized with sodium pento- barbital (30 mg/kg, iv). After endotracheal http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Heart and Circulatory Physiology The American Physiological Society

Inhibition of endo- and epicardial glycogenolysis by propranolol in ischemic hearts

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Publisher
The American Physiological Society
Copyright
Copyright © 1977 the American Physiological Society
ISSN
0363-6135
eISSN
1522-1539
Publisher site
See Article on Publisher Site

Abstract

IN THE PREVIOUS PAPER (7) we have demonstrated in open-chest dogs that coronary artery elevated the phosphorylase activity and accelerated the breakdown of glycogen in the region of left ventricular wall that had been perfused by the ligated coronary artery, and we have also reported that the coronary artery -induced acceleration in metabolism in the endocardial layers was more rapid and marked than that in the epicardial. The mechanisms by which coronary artery produces acceleration of myocardial glycogenolysis, however, are not fully elucidated. Several investigators (5, 8, 18) have suggested that catecholamine release occurs in response to ischemia in the myocardium. If catecholamine release occurs after coronary artery in the region of myocardium that has been perfused by the coronary artery, it is possible to assume that the coronary artery -induced acceleration of phosphorylase activity and breakdown of glycogen in the dog myocardium would be inhibited by pretreatment of the dog with a beta-adrenergic blocking agent. The present study, therefore, was undertaken to examine the above assumption using propranolol as a beta-adrenergic blocking agent. MATERIALS AND METHODS Animal preparation. Mongrel dogs of either sex weighing 7-15 kg were anesthetized with sodium pento- barbital (30 mg/kg, iv). After endotracheal

Journal

AJP - Heart and Circulatory PhysiologyThe American Physiological Society

Published: Apr 1, 1977

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