Abstract
Ischaemic myocardial tissue will, inevitably, necrose if blood flow is not restored. Whilst reperfusion is always beneficial in terms of potential recovery of heart muscle, reperfusion in itself is believed to bring about cellular injury. While the causes of this 'reperfusion injury' are apparently multifactorial, there is now an increasing body of evidence to suggest that oxygen free radicals play a major role in the pathogenesis of reperfusion injury. The initial evidence for this hypothesis was indirect, based on the ability of free radical scavengers to limit myocardial injury in animal models. More recent work has utilised the highly specific technique of electron spin resonance (ESR) spectroscopy and ESR spin trapping to detect the free radical species. The evidence for free radical production on myocardial reperfusion will be presented along with details of human studies. The potential for a therapeutic intervention will also be briefly discussed.
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