Nitric oxide release from coronary vasculature before, during, and following cardioplegic arrest

Nitric oxide (NO) is known as a vasodilatory molecule synthesized by vascul ar endothelium. The NO-dependent vasodilatory response of coronary artery i s impaired after ischemia and reperfusion. In the present study, the releas e of NO from coronary vasculature was evaluated before and during cardiople gic arrest and after reperfusion. Nine patients undergoing heart surgery we re studied. Multidose crystalloid cardioplegics were used for myocardial pr otection. The coronary affluent and effluent were obtained simultaneously b efore cardioplegic arrest, at each cardioplegic administration, and after r eperfusion; and the levels of nitrite and nitrate, the stable end-products of NO, were measured. The NO release from the coronary vasculature was dete rmined as the difference in the levels of nitrite and nitrate between the c oronary effluent and affluent. The level of nitrite/nitrate release from co ronary vasculature was 6.8 +/- 3.7 mu M before cardioplegic arrest. During cardioplegic arrest the nitrite/nitrate release decreased, reaching 1.3 +/- 1.3 mu M (p < 0.05, vs. before cardioplegic arrest) at the fourth administ ration of the cardioplegic. At 3 to 5 minutes after reperfusion, nitrite/ni trate release further decreased to 0.36 +/- 0.34 mu M (p < 0.05, vs. before cardioplegic arrest). During cardioplegic arrest the NO release decreased and reached significance at approximately 70 minutes of cardioplegic arrest compared to that before cardioplegic arrest. After reperfusion, NO release was further reduced, with statistical significance compared to that before cardioplegic arrest. Our data may indicate that cardioplegic arrest and re perfusion cause endothelial dysfunction.