The effect of verapamil on mechanical performance of acutely ischemic and reperfused myocardium in the conscious dog.

Abstract

The effect of verapamil, an inhibitor of transmembrane calcium flux, was studied in intact conscious dogs with myocardial ischemia produced by inflating a balloon cuff implanted on the left anterior descending coronary artery. Six dogs received a continuous infusion of verapamil (10 microgram/kg per min) beginning prior to coronary occlusion, and six received normal saline infusions. Systolic ejection shortening (SES) was measured from subendocardial ultrasonic crystals implanted in the central ischemic zone (IZ) and border zone (BZ), and in a nonischemic control zone (CZ). Hearts were paced at a constant heart rate with periodic introduction of closely coupled extrasystoles. SES was measured both for normally paced beats and during postextrasystolic potentiation (PESP). Regional myocardial blood flow was measured by injecting radioactive microspheres before, during, and after coronary occlusion. There were no significant differences between verapamil-treated dogs and saline control dogs in mean aortic pressure, heart rate, left ventricular end-diastolic pressure or dP/dt, cardiac output, or regional myocardial blood flow in IZ, BZ, or CZ. Differences in mechanical performance between two groups were noted, however. In the IZ, SES was abolished completely for normally paced beats in both groups but was significantly preserved for PESP beats in the verapamil-treated animals. In the BZ, SES was significantly reduced for normally paced beats only in the saline controls, and PESP responses were preserved to a significantly greater degree in the verapamil-treated animals. These results indicate that verapamil pretreatment exerts beneficial effects upon mechanical performance of ischemic myocardium. Since no changes in systemic hemodynamics or regional myocardial blood flow were observed, the effect may be due to the calcium-antagonistic properties of the agent.