Sotalol and infarct size after coronary ligation in the baboon

We investigated the hemodynamic effects and myocardial salvage actions of sotalol during experimental myocardial infarction in the baboon. Ten baboons received placebo and six were given sotalol. In anesthetized open-chest baboons base-line determinations included heart rate (HR), rate-pressure product (RPP), left ventricular dP/dt, aortic pressures, serum creatine kinase MB isoenzyme (CK-MB) activity, and a 16-point epicardial ST segment map. The left anterior descending coronary artery was then ligated and the measurements were repeated at 15-min and at 2-h intervals up to 12 h after occlusion. At 12 h, coronary blood flow and myocardial CK activity were also measured. Twenty minutes after ligation, either sotalol (3 mumol . kg-1 followed by 2 nmol . kg-1 . min-1) or placebo (saline) was administered intravenously. Sotalol reduced HR but not dP/dt or the degree of afterload. The reduction in HR resulted in a significant decrease in RPP (myocardial O2 consumption). Sotalol administration also resulted in a decrease in coronary blood flow (myocardial O2 supply). There were no significant differences between the two groups in serum CK-MB activity or in the extent of myocardial damage, as predicted by the 15-min ST-segment deviations and myocardial CK activity at 12 h. The reduction in myocardial oxygen demand caused by sotalol was accompanied by a decrease in oxygen supply. As a consequence, no significant reduction in myocardial ischemic damage was found in the group given sotalol.