title: Protective role of increased myocardial glycogen stores induced by propranolol.
abstract: Glycogen is an essential substrate during myocardial anoxia. Since porpranolol may maintain myocardial glycogen levels after acute stress by blockade of catecholamine-induced glycogenolysis, we evaluated the effect of propranolol treatment in the isolated perfused isovolumic paced rat heart. Forty-one rats were studied after 10 min of ice-water immersion: half were pretreated with propranolol, 20 mg/kg/day x3, and half with saline. Glycogen content of unperfused propranolol-treated hearts exceeded controls by 46% (146 +/- 9 vs. 100 +/- 4 mumoles/g dry wt, p less than 0.02), and this difference persisted during aerobic perfusion. Propranolol did not affect adenine nucleotide concentration or left ventricular hemodynamics. Following 5 min of anoxic perfusion, propranolol hearts showed improved ventricular performance concomitant with enhanced glycogenolytic flux and lactate production. Propranolol augmented high energy phosphate production (ATP/AMP = 5.19 +/- 0.42 vs. 3.39 +/- 0.42, p less than 0.02) and increased coronary flow (22.1 +/- 1.6 vs. 16.6 +/- 1.4 ml/min, p less than 0.02) during anoxia. Thus, propranolol supported glycogen stores following acute stresses, enhanced glycogenolytic energy production, increased coronary flow, and improved ventricular function during subsequent anoxia.
mesh_terms: D000818:Animals; D002395:Catecholamines / Q000378:metabolism; D003326:Coronary Circulation / Q000187:drug effects; D006003:Glycogen / Q000378:metabolism*; D006439:Hemodynamics / Q000187:drug effects*; D000860:Hypoxia / Q000503:physiopathology; D007773:Lactates; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010477:Perfusion; D010710:Phosphates / Q000378:metabolism; D011433:Propranolol / Q000494:pharmacology*; D051381:Rats; D014867:Water / Q000378:metabolism
chemical_list: D002395:Catecholamines; D007773:Lactates; D010710:Phosphates; D014867:Water; D006003:Glycogen; D011433:Propranolol