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Am J Physiol Heart Circ Physiol 260: H805-H810, 1991;
0363-6135/91 $5.00
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AJP - Heart and Circulatory Physiology, Vol 260, Issue 3 805-H810, Copyright © 1991 by American Physiological Society

ARTICLES

Existence and participation of xanthine oxidase in reperfusion injury of ischemic rabbit myocardium

L. S. Terada, J. D. Rubinstein, E. J. Lesnefsky, L. D. Horwitz, J. A. Leff and J. E. Repine
Webb-Waring Lung Institute, Denver, Colorado.

Using a highly specific assay that minimizes enzyme inactivation in vitro, we found that rabbit myocardial tissue contained low levels of xanthine oxidase (XO) and xanthine dehydrogenase (XD) activity that were effectively inhibited by pretreatment of hearts with allopurinol. In parallel, allopurinol treatment also improved ventricular developed pressure, peak systolic pressure, and coronary flow in isolated hearts subjected to 30 min of normothermic global ischemia and 30 min of reperfusion. Although function was protected by allopurinol treatment, creatine kinase (CK) release was not altered by allopurinol. Inhibition of myocardial XO with allopurinol did not increase myocardial ATP or phosphocreatine. In addition, allopurinol did not scavenge superoxide anion or hydrogen peroxide in vitro. The results support the possibility that relatively low amounts of XO activity, similar to levels reported in human myocardium, may contribute to cardiac ischemia-reperfusion injury.


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M. Houston, A. Estevez, P. Chumley, M. Aslan, S. Marklund, D. A. Parks, and B. A. Freeman
Binding of Xanthine Oxidase to Vascular Endothelium. KINETIC CHARACTERIZATION AND OXIDATIVE IMPAIRMENT OF NITRIC OXIDE-DEPENDENT SIGNALING
J. Biol. Chem., February 19, 1999; 274(8): 4985 - 4994.
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