Myocardial Salvage by the Free Radical Scavenging Actions of Xanthine Oxidase Inhibitors
It is well established that oxygen-derived free radicals play a crucial role in the pathogenesis of ischemic-reperfusion injury.1 However, the source of these radicals remains unknown. McCord2 has proposed that oxygen radicals are generated during reoxygenation of ischemic myocardium by the action of xanthine oxidase on hypoxanthine. A number of investigators supported this hypothesis based on their observations of allopurinol-mediated reduction of reperfusion injury.3 Recently, the beneficial action of allopurinol to salvage ischemic-reperfused myocardium has been challenged by Reimer et al.4 In addition, most of the mammalian hearts, with the exception of rat heart, have been found to contain negligible or no xanthine oxidase activity at all.5 The purpose of the present study was, therefore, to investigate the role of two xanthine oxidase inhibitors, allopurinol and oxypurinol, on the ischemic-reperfused heart and to explore their mechanisms of action. Our results suggest that these xanthine oxidase inhibitors salvage the ischemic-reperfused myocardium by scavenging the free radicals.
KeywordsElectron Paramagnetic Resonance Electron Paramagnetic Resonance Spectrum Xanthine Oxidase Electron Paramagnetic Resonance Signal Xanthine Oxidase Activity
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