Impaired endothelium-dependent relaxation after cardiac global ischemia and reperfusion: role of warm blood cardioplegia

Division of Thoracic and Cardiovascular Surgery, Chang Gung Memorial Hospital, Chang Gung Medical College, Taipei, Taiwan, Republic of China.

OBJECTIVES: Experiments were designed to determine whether coronary endothelial dysfunction after cardiac global ischemia and reperfusion could be prevented by warm blood cardioplegic solution. BACKGROUND: The coronary endothelium produces endothelium-derived relaxing factor (EDRF) 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 circulation 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 cardioplegic solution (group 1) or intermittent cold (4 degrees C) crystalloid cardioplegic solution was not used in group 3 animals. The heart was then 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 significantly different from that of groups 2 and 3 but was not significantly different from that of group 4. In contrast, EDR in response to the receptor-independent calcium ionophore agonist A23187 was not significantly different between the four groups. Scanning electron microscopic studies 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 dysfunction. This type of coronary endothelial dysfunction can be prevented by continuous anterograde infusion of warm blood cardioplegic solution during global ischemia.

This article has been cited by other articles:

				K. Yamazaki, S. Miwa, K. Ueda, S. Tanaka, S. Toyokuni, O. Unimonh, K. Nishimura, and M. Komeda Prevention of myocardial reperfusion injury by poly(ADP-ribose) synthetase inhibitor, 3-aminobenzamide, in cardioplegic solution: in vitro study of isolated rat heart model Eur. J. Cardiothorac. Surg., August 1, 2004; 26(2): 270 - 275. [Abstract] [Full Text] [PDF]

				A. Serraf, H. Aznag, B. Baudet, H. Detruit, F. Seccatore, M. G. Mazmanian, and C. Planche Pulmonary vascular endothelial growth factor and nitric oxide interaction during total cardiopulmonary bypass in neonatal pigs J. Thorac. Cardiovasc. Surg., May 1, 2003; 125(5): 1050 - 1057. [Abstract] [Full Text] [PDF]

				C.-H. Yeh, Y.-C. Wang, Y.-C. Wu, J.-J. Chu, and P. J. Lin Continuous Tepid Blood Cardioplegia Can Preserve Coronary Endothelium and Ameliorate the Occurrence of Cardiomyocyte Apoptosis Chest, May 1, 2003; 123(5): 1647 - 1654. [Abstract] [Full Text] [PDF]

				A. Parolari, P. Rubini, A. Cannata, L. Bonati, F. Alamanni, E. Tremoli, and P. Biglioli Endothelial damage during myocardial preservation and storage Ann. Thorac. Surg., February 1, 2002; 73(2): 682 - 690. [Abstract] [Full Text] [PDF]

				N. Hayashida, S. Chihara, E. Tayama, S. Yokose, K. Akasu, E. Kai, and S. Aoyagi Effects of angiotensin-converting enzyme inhibitor during warm blood cardioplegia Ann. Thorac. Surg., August 1, 2000; 70(2): 627 - 632. [Abstract] [Full Text] [PDF]