Abstract

Much evidence has accumulated implicating cytotoxic free radicals as an underlying etiology of many clinical disorders. Prominent among these dis­ orders has been ischemic heart disease (25,57). The bulk of the incriminating evidence has been based on the ability of antioxidants to reduce injury in animal models of myocardial ischemia. Unfortunately, quantifying myocar­ dial injury is still an imprecise science and, as a result, the performance of the various antioxidant interventions has varied widely in the different models. Because of the discrepant data, it has been impossible to determine the exact role that free radicals play in the ischemic heart or what long-term clinical benefit might be derived from an antioxidant intervention in the ischemic patient. Although it is well-established that some free radicals are produced on reperfusion of the ischemic heart, it is the magnitude of the injury that the radicals produce that remains in question. Although the in vitro work has established a theoretical framework for the free radical hypothesis, in the final analysis this question will only be answered by measuring the protection derived in a whole animal by an antioxidant intervention. Unfortunately, the gaps in our understanding of any new theory have to be

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