Lack of protection of ischemic myocardium by verapamil in conscious dogs.
To determine whether coronary dilatation and decreased myocardial oxygen requirements resulting from administration of verapamil, a calcium and slow current antagonist, protect ischemic myocardium in conscious dogs, we studied 15 treated and 15 control animals after coronary occlusion. Verapamil (0.2-0.7 mg/kg/h) was given by continuous infusion for 17 h beginning 5 h after the initial plasma creatine kinase (CK) elevation after coronary occlusion. Observed infarct size and infarct size predicted before verapamil were estimated from hourly plasma CK values and infarct size was estimated also from myocardial CK depletion measured directly, 24 h after occlusion. Changes in heart rate, blood pressure, and frequency of premature ventricular complexes (recorded every 30 min) after occlusion were similar in treated and control dogs. Coronary flow after verapamil, measured with radioactively labeled microspheres, did not increase in ischemic zones but increased by 90% in normal myocardium (p less than 0.05). The differences between observed and predicted infarct size estimated from plasma CK changes in treated and controls were similar (3.0 +/- 2.2 (S.E.) and 2.0 +/- 1.4 CK-g-eq), and myocardial CK depletion was also comparable in the two groups (25 +/- 2% and 23 +/- 2%). Thus although verapamil, administered five hours after the initial plasma CK elevation, increased coronary flow in normal myocardium, it did not augment flow in ischemic tissue or limit the extent of infarction.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D003326:Coronary Circulation / Q000187:drug effects; D003402:Creatine Kinase / Q000097:blood / Q000378:metabolism; D004285:Dogs; D006339:Heart Rate / Q000187:drug effects; D009203:Myocardial Infarction / Q000201:enzymology / Q000503:physiopathology*; D009206:Myocardium / Q000201:enzymology; D014700:Verapamil / Q000494:pharmacology*
D014700:Verapamil; D003402:Creatine Kinase