Effects of nicardipine on ischemic mechanical failure and tissue injury in isolated perfused rat heart.

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Using a Langendorff rat heart preparation, we examined effects of nicardipine, a calcium channel blocker, on different stages of ischemic damage, characterized by a development of contracture and leakage of intracellular enzymes. Maximum recoveries of heart rate (HR) and peak left ventricular pressure-HR product, after 20min ischemia were attenuated by about 25% compared with those before ischemia. When nicardipine (0.1μmol) was added to the perfusate 5min prior to ischemia, this mechanical failure recovered completely to the pre-ischemic level. Although a significant increase in left ventricular end-diastolic pressure was observed in hearts exposed to 30min ischemia, the amount of creatine kinase (CK) released during re-flow after 30min ischemia was not enhanced by contracture but was proportional to the duration of ischemia (compared with that of 20min ischemia). Nicardipine reduced CK leakage by 25% after 30min ischemia but did not alter either ATP levels or coronary flow. The beneficial effects of nicardipine on ischemic damage are probably related to inhibition of calcium influx (Terai et al: Biochem Pharmacol 30: 375, 1981), which may accompany reperfusion of ischemic myocardium.
International Heart Journal刊行会の論文