The efficacy of benidipine hydrochloride in preventing myocardial ischemia and reperfusion injury was evaluated in isolated rabbit hearts (n = 28). Isovolumic left ventricular function, coronary flow, creatine phosphokinase (CPK) release, and myocardial water content were measured after ischemia during both normothermia (37 degrees C; Group I) and hypothermia (23 degrees C; Group II). After baseline measurements, hearts were induced to arrest by chilled cardioplegic solution. Each group was divided into two subgroups, depending upon whether benidipine hydrochloride (10(-9) mole/liter) was added in the cardioplegia (A, without benidipine; B, with benidipine). After 30 min of ischemia for Group I and 180 min for Group II (which added another cardioplegia every 30 min), hearts were reperfused. Measurements the same as those at baseline were carried out every 15 or 30 min for up to 60 min. Benidipine-treated hearts started beating in a shorter time than did control hearts (Group I-B, 38.7 +/- 3.7 sec vs Group I-A, 59.9 +/- 5.6; Group II-B, 36.7 +/- 2.0 vs Group II-A, 47.8 +/- 3.3). The percentage of recovery of left ventricular developed pressure after 60 min of reperfusion was significantly better in benidipine groups (P < 0.05). With respect to changes in coronary flow and CPK release after reperfusion, benidipine groups were preserved extremely well. We conclude that the addition of benidipine hydrochloride to cardioplegic solution significantly improves ventricular function after myocardial ischemia and reperfusion.