Failure of high doses of propranolol to reduce experimental myocardial ischemic damage.
Myocardial creatine phosphokinase (CPK) activity and myocardial blood flow (MFB, 15 +/- mu microspheres) were measured at 24 hours after ligation of the left anterior descending coronary artery in nine untreated anesthetized dogs, in eight dogs pretreated with intravenous propranolol 5 mg/kg and in eight which had both pretreatment as well as infusion of propranolol (1.25 mg/kg/hour) after occlusion. Loss of CPK activity from the border and center zones of the myocardial infarct was similar in extent in dogs which had pretreatment but no infusion of propranolol as it was in the control group. Loss of CPK from the center zone was greater (P less than 0.005) in dogs receiving pretreatment followed by constant infusion of the drug. Propranolol had no significant effect on collateral blood flow to the border or center zone of the infarct. In separate experiments, there was no important difference in hemodynamic measurements, except a slower heart rate (P less than 0.01), when pretreated dogs were compared with control dogs up to 2 hours after coronary ligation. We conclude that propranolol given in this dose does not influence nyocardial damage, on the basis of regional myocardial blood flow or tissue CPK depletion values at 24 hr after coronary occlusion.
D000818:Animals; D003326:Coronary Circulation; D003327:Coronary Disease / Q000517:prevention & control*; D003402:Creatine Kinase; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004562:Electrocardiography; D006439:Hemodynamics / Q000187:drug effects; D011433:Propranolol / Q000097:blood / Q000627:therapeutic use*; D014693:Ventricular Fibrillation / Q000188:drug therapy
D011433:Propranolol; D003402:Creatine Kinase