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

Abstract

Nitric oxide (NO) is known as a vasodilatory molecule synthesized by vascular endothelium. The NO-dependent vasodilatory response of coronary artery is impaired after ischemia and reperfusion. In the present study, the release of NO from coronary vasculature was evaluated before and during cardioplegic arrest and after reperfusion. Nine patients undergoing heart surgery were studied. Multidose crystalloid cardioplegics were used for myocardial protection. The coronary affluent and effluent were obtained simultaneously before cardioplegic arrest, at each cardioplegic administration, and after reperfusion; and the levels of nitrite and nitrate, the stable end-products of NO, were measured. The NO release from the coronary vasculature was determined as the difference in the levels of nitrite and nitrate between the coronary effluent and affluent. The level of nitrite/nitrate release from coronary vasculature was 6.8 +/- 3.7 microM before cardioplegic arrest. During cardioplegic arrest the nitrite/nitrate release decreased, reaching 1.3 +/- 1.3 microM (p < 0.05, vs. before cardioplegic arrest) at the fourth administration of the cardioplegic. At 3 to 5 minutes after reperfusion, nitrite/nitrate release further decreased to 0.36 +/- 0.34 microM (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 reperfusion cause endothelial dysfunction.