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 "terminal 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 into three groups: in group A (n = 10) the hearts reperfused without any treatment; in group B (n = 9) the hearts received coronary perfusion 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) the hearts received coronary perfusion with Nicorandil-Mg free solution (glucose, 50 g/l). During and after ischemia, the myocardial tissue PCO2 (t-PCO2) was continuously monitored by an ion-sensitive field effective transistor (ISFET) sensor. In addition, the myocardial tissue blood flow (TBF), oxygen consumption, and lactate flux were then calculated at 5, 10, 20, and 40 min of reperfusion. In the initial reperfusion 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 < 0.025; 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 reperfusion (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.(ABSTRACT TRUNCATED AT 250 WORDS)