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J Thorac Cardiovasc Surg 1994;107:1222-1227
© 1994 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

Xanthine oxidoreductase release after descending thoracic aorta occlusion and reperfusion in rabbits

Birmingham, Ala., and Cambridge, Mass.

Partially supported by the National Institutes of Health grant HL 48676.

Received for publication June 17, 1993. Accepted for publication Sept. 14, 1993. Address for reprints: V. G. Nielsen, MD, Department of Anesthesiology, Research Division, University of Alabama at Birmingham, 845 Jefferson Tower, 619 S. 19th St., Birmingham, AL 35233-6810.

Abstract

Cardiopulmonary and other organ dysfunction often occurs after operation on the descending thoracic aorta. Though there are multiple causes of organ dysfunction in this setting, free radical injury may play a prominent role. Xanthine oxidoreductase, an enzyme that generates oxidants after exposure to ischemia, could be released from ischemic liver and intestine during reperfusion. To test this hypothesis, we created aortic occlusion in eight rabbits for 40 minutes by inflation of a 4F Fogarty balloon catheter in the descending thoracic aorta. Eight sham-operated rabbits served as a control group. Two hours of reperfusion followed removal of the balloon catheter. Hemodynamic and acid-base status were maintained near baseline values during reperfusion. Plasma samples were obtained for determination of the activity of the hepatocellular enzymes xanthine oxidoreductase, aspartate aminotransferase, alanine transferase, and lactate dehydrogenase. Plasma xanthine oxidoreductase activity increased significantly (p < 0.001) during reperfusion (729 ± 140µU/ml, mean ± standard error of the mean) compared with baseline (132 ± 18µU/mL). The other enzymes followed a similar pattern of release. We report the release of xanthine oxidoreductase in an animal model that simulates the situation of human thoracic aorta operations. The oxidants produced by the circulating xanthine oxidoreductase observed during reperfusion would likely be toxic to vascular endothelium, potentially contributing to multiple organ dysfunction. (J THORACCARDIOVASCSURG1994;107:1222-7)

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