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J Thorac Cardiovasc Surg 1997;114:100-108
© 1997 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

CONTINUOUS ANTEGRADE WARM BLOOD CARDIOPLEGIA ATTENUATES AUGMENTED CORONARY ENDOTHELIUM–DEPENDENT CONTRACTION AFTER CARDIAC GLOBAL ISCHEMIA AND REPERFUSION

Supported by grant CMRP 421 from the Chang Gung Memorial Hospital, Chang Gung Medical College, and in part by grant NSC85-2331-B-182-012 from the National Science Council, Executive Yuan, Taiwan, Republic of China.

Received for publication August 20, 1996. revisions requested Oct. 8, 1996; revisions received Nov. 13, 1996 accepted for publication Dec. 27, 1996. Address for reprints: Pyng Jing Lin, MD, Division of Thoracic and Cardiovascular Surgery, Chang Gung Memorial Hospital, 199, Tun-Hwa North Rd., Taipei, Taiwan, Republic of China.

Abstract

Background: Experiments were designed to evaluate the effect of warm blood cardioplegia on endothelium-dependent contraction of the coronary endothelium after cardiac global ischemia and reperfusion. Method: Dogs (n = 12 in each group) were exposed to extracorporeal circulation with the body temperature at 37° C (group 1) or 28° C (groups 2 and 3). The ascending aorta was crossclamped for 120 minutes while continuous infusion of warm blood cardioplegec solution (group 1) or intermittent infusion of cold (4° C) crystalloid cardioplegic solution (group 2) was performed via the coronary arteries through the aortic root. Cardioplegic solution was not used in group 3 animals. The heart was then allowed to function for 60 minutes of reperfusion. Reperfused (groups 1, 2, and 3) and control (group 4) coronary arteries were then harvested for study. Results: Perfusate hypoxia caused endothelium-dependent contraction in the arteries of all four groups that could be attenuated by N^G-monomethyl-L-arginine (L-NMMA) or L-NMMA plus D-arginine, but not by L-NMMA plus L-arginine or endothelin receptor A and B antagonist PD 145065. The endothelium-dependent contraction results in groups 2 and 3 (75% ± 4% and 80% ± 5%, respectively) were significantly greater than those in groups 1 and 4 (15% ± 3% and 18% ± 5%, respectively). Scanning electron microscope studies showed that platelet adhesion and aggregation, areas of microthrombi, disruption of endothelial cells, and separation of the intercellular junction could be found in coronary segments from groups 2 and 3, but not in vessels from groups 1 and 4. Conclusion: These experiments suggest that global ischemia and reperfusion enhances hypoxia-mediated endothelium-dependent contraction of the coronary endothelium and damages the ultrastructure. These kinds of changes can be prevented by continuous antegrade infusion of warm blood cardioplegic solution during global ischemia