Reperfusion of the heart after induced myocardial ischemia may be associated with severe myocardial damage, characterized by massive calcium influx and accumulation in the heart cells. The present study was undertaken to investigate whether verapamil, a slow channel calcium blocker, administered prior to reperfusion, might reduce this reflow injury without causing depression of heart function. Thirty-two isolated, perfused rabbit hearts were subjected either to 45 minutes of normothermic or 150 minutes of hypothermic global ischemia. Half of the hearts in each group received verapamil immediately prior to reperfusion, while the remaining hearts received no verapamil. Following ischemia and 60 minutes of reperfusion, left ventricular (LV) contractility was superior in both groups of verapamil-treated hearts, compared to control hearts (LV developed pressure [DP] in normothermic hearts 63 ± 6% of preischemic DP for verapamil-treated hearts versus 46 ± 6% of preischemic DP for control hearts; in the hypothermic group, 65 ± 8% of preischemic DP for verapamil-treated hearts versus 33 ± 70% DP for control hearts). Postischemic LV compliance also was significantly improved in the verapamil-treated hearts throughout the period of reperfusion, compared to control hearts. No differences were noted in coronary flow, myocardial water content, or the onset of electromechanical activity between the verapamil and control hearts, but there was significantly improved ultrastructural preservation in both verapamil groups. These data demonstrate that verapamil, when administered just prior to reperfusion, results in improved recovery of myocardial function and excellent cellular preservation, presumably by reducing calcium influx into myocardial cells.
|Original language||English (US)|
|Number of pages||8|
|State||Published - Aug 1983|
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