Influence of propranolol on acidosis and high energy phosphates in ischaemic myocardium of the rabbit.
Catecholamines stimulate adenosine triphosphate consumption and glycogenolysis in isolated hearts. In ischaemic myocardium a protective effect of beta adrenergic blockade may therefore arise from reduced adenosine triphosphate consumption or attenuation of acidosis. To characterise the biochemical mechanism of this protective effect phosphorus metabolite concentrations and intracellular pH were measured in an ischaemic region of the rabbit heart in vivo using 31P-nuclear magnetic resonance spectroscopy. After occlusion of the left anterior descending coronary artery there was a rapid decrease in intracellular phosphocreatine concentrations, and intracellular adenosine triphosphate concentrations decreased at a rate of approximately 0.5 mumol X g-1 dry weight X min-1. Intracellular pH decreased approximately linearly to a final pH of about 5.8. In the ischaemic myocardium of the animals treated with propranolol the intracellular concentrations of adenosine triphosphate were higher and those of phosphocreatine lower and the pH was the same compared with control after 30 minutes of ischaemia. Thus any protective effect of propranolol in vivo is not associated with attenuation of intracellular acidosis in this preparation.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003327:Coronary Disease / Q000378:metabolism*; D006863:Hydrogen-Ion Concentration; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008660:Metabolism / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism*; D010710:Phosphates / Q000378:metabolism*; D010725:Phosphocreatine / Q000378:metabolism; D011433:Propranolol / Q000494:pharmacology*; D011817:Rabbits
D010710:Phosphates; D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D011433:Propranolol