PREVENTION OF POSTISCHEMIC REPERFUSION INJURY - THE IMPROVEMENT OF MYOCARDIAL TISSUE BLOOD-FLOW AFTER ISCHEMIA BY TERMINAL NICORANDIL-MG CARDIOPLEGIA

We evaluated the preventive effect of postischemic reperfusion injury by Nicorandil-Mg cardioplegia given just prior to reperfusion as ''ter minal cardioplegia.'' Twenty seven dogs were placed on cardiopulmonary bypass and the aorta was cross-clamped for 90 min under hypothermic ( 17-19-degrees-C) cardioplegic arrest. The canine hearts were divided i nto three groups: in group A (n = 10) the hearts were reperfused witho ut any treatment; in group B (n = 9) the hearts received coronary perf usion with Nicorandil-Mg solution (Nic, 8 mg/l; Mg, 20 mEq/l; glucose, 50 g/l) for 2 min just prior to reperfusion; and in group C (n = 8) t he hearts received coronary perfusion with Nicorandil-Mg free solution (glucose, 50 g/l). During and after ischemia, the myocardial tissue P CO2 (t-PCO2) was continuously monitored by an ion-sensitive field effe ctive transistor (ISFET) sensor. In addition, the myocardial tissue bl ood flow (TBF), oxygen consumption, and lactate flux were then calcula ted at 5, 10, 20, and 40 min of reperfusion. In the initial reperfusio n period, Group B showed an improved TBF compared to group A and C (at 5 min, group B was 42.7 +/- 11.9; group A was 29.4 +/- 11.2, P < 0.02 5; and group C was 33.9 +/- 9.2% of the preischemic control level, P < 0.05). T-PCO2 in group B was significantly decreased at 5 min of repe rfusion (group B, 127.5 +/- 22.5 --> 42.5 +/- 9.7; group A, 117.5 +/- 23.0 --> 85.2 +/- 17.4, P < 0.001; group C, 122.3 mmHg --> 68.2 +/- 18 .7 mmHg, P < 0.01), and group B had a better metabolic recovery. These results suggest that terminal Nicorandil-Mg cardioplegia might reduce the rate of postischemic reperfusion injury.