IMPAIRED ENDOTHELIUM-DEPENDENT RELAXATION AFTER CARDIAC GLOBAL-ISCHEMIA AND REPERFUSION - ROLE OF WARM BLOOD CARDIOPLEGIA

Objectives. Experiments were designed to determine whether coronary en dothelial dysfunction after cardiac global ischemia and reperfusion co uld be prevented by warm blood cardioplegic solution. Background. The coronary endothelium produces endothelium-derived relaxing factor (EDR F) to prevent vasospasm and thrombosis. After ischemia and reperfusion , endothelium-dependent relaxation (EDR) is diminished as a result of G-protein dysfunction. Methods. Dogs were exposed to extracorporeal ci rculation in 37 degrees C (group 1) or 28 degrees C (groups 2 and 3). The heart was ischemic for 120 min while continuous warm blood cardiop legic solution (group 1) or intermittent cold (4 degrees C) crystalloi d cardioplegic solution (group 2) was infused into the aortic root. Ca rdioplegic solution was not used in group 3 animals, The heart was the n allowed to function for 60 min of reperfusion. Results. Endothelium- derived relaxation in response to acetylcholine, adenosine diphosphate and sodium fluoride of the coronary rings of group 1 was significantl y different from that of groups 2 and 3 but was not significantly diff erent from that of group 4. In contrast, EDR in response to the recept or-independent calcium ionophore agonist A23187 was not significantly different between the four groups. Scanning electron microscopic studi es showed that platelet adhesion and aggregation, area of microthrombi , disruption of endothelial cells and separation of the intercellular junction could be found in coronary segments of groups 2 and 3 but not in vessels of groups 1 and 4. Conclusions. These experiments suggest that cardiac global ischemia and reperfusion impair receptor-mediated release of EDRF from the coronary endothelium with G-protein dysfuncti on. This type of coronary endothelial dysfunction can be prevented by continuous anterograde infusion of warm blood cardioplegic solution du ring global ischemia. (C) 1997 by the American College of Cardiology.