Direct metabolic effects of isoproterenol and propranolol in ischemic myocardium of the dog.
The effect of either isoproterenol or propranolol on the metabolism of ischemic myocardium was examined. To ensure that all changes were due to changes in metabolism and not drug-induced changes in residual flow to the ischemic regions, we devised a preparation in which two coronary branches on the same heart were simultaneously perfused at a low flow rate. Microsphere measurements verified that the two ischemic regions were receiving identical blood flow rates. One branch received an infusion of 0.9% NaCl and the other received the drug. After 1 h both regions were biopsied and the high-energy phosphate levels in each region were determined. ATP and phosphocreatine each fell to about 50% of their starting values in the 0.9% NaCl-treated regions, and isoproterenol did not further depress the high-energy phosphate concentrations. Propranolol, on the other hand, significantly preserved the high-energy phosphate concentrations. We conclude that although isoproterenol seemed incapable of accelerating energy utilization in ischemic myocardium, propranolol is apparently capable of reducing it.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects*; D004285:Dogs; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D007545:Isoproterenol / Q000494:pharmacology*; D008297:Male; D009206:Myocardium / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism; D011433:Propranolol / Q000494:pharmacology*
D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D011433:Propranolol; D007545:Isoproterenol