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Evidence of a reversible oxygen radical mediated component of reperfusion injury: Reduction by recombinant human superoxide dismutase administered at the time of reflow
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Recombinant superoxide dismutase reduces oxygen free radical concentrations in reperfused myocardium
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Substrate control of free radical generation from xanthine oxidase in the postischemic heart
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Cardioprotection by Cu, Zn-superoxide dismutase is lost at high doses in the reoxygenated heart
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Superoxide dismutase reduces reperfusion arrhythmias but fails to salvage regional function or myocardium at risk in conscious dogs
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