Nifedipine, an antagonist of myocardial calcium uptake, given after a period of a cold, cardioplegic arrest (150 min, 18 degrees C, St Thomas' cardioplegic solution) improved contractile recovery of the isolated working rat heart model of cardiopulmonary bypass. The hearts were reperfused with various concentrations of nifedipine in Krebs-Henseleit buffer (37 degrees C, 100 cm H2O) and their functional recoveries were compared with the control series reperfused without nifedipine. A bell-shaped dose/response curve was produced by the drug, and optimal protection observed with 0.1 mumol/l of nifedipine which improved the post-ischaemic recovery of the aortic flow from 56.8% +/- 3.7% to 80.1% +/- 3.2% (P less than 0.001). The importance of careful dose adjustment is stressed since it was noted that higher concentrations inhibit both functional and metabolic performance. This study supports the hypothesis that at the end of a cold cardioplegic arrest there are still reversibly injured cells which could restore their function if the cellular ingress of Ca++ during reperfusion is reduced by nifedipine.
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