Abstract
It is now well established that reperfusion of ischemic heart tissues initiates the production of oxygen free radicals which exacerbate the damage to the myocardium (1–3). While it is clear that a large portion of the oxygen free radicals is formed in damaged tissue by endogenous reactions such as the metabolism of xanthine and arachidonic atld (4,5), it now appears likely that a major source of these free radicals are the neutrophils which migrate into the damaged tissues during the inflammatory response (6–8). At the site of damage, these neutrophils can become activated and can secrete a variety of oxidants such as superoxide anion, hydrogen peroxide, and hypochlorous acid (9).
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