Key result
Post-ischaemic reperfusion injury is mediated by oxygen radicals and neutrophils, leading to oxidative tissue damage, microvascular impairment, and no-reflow despite adequate epicardial flow.
This review highlights the mechanisms of myocardial reperfusion injury, emphasizing the roles of oxygen radicals and neutrophils in causing microvascular impairment despite epicardial reflow.
Post-ischaemic reperfusion carries an injurious component that may partly counteract the beneficial effects of reflow; this component has been termed ‘reperfusion injury’. Principal mediators of this phenomenon are oxygen radicals and neutrophils. Oxygen radicals, generated in large amounts upon reflow, induce oxidative tissue damage and modulate various events that ultimately lead to tissue injury; neutrophil activation is accompanied by release of lytic, pro-inflammatory and vasoconstricting molecules, and they may plug capillaries. Flow may thus be impaired at the microvascular level, despite adequate flow in epicardial arteries (‘no-reflow’). These phenomena represent a ubiquitous reaction of tissues to ischaemia and reflow.
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Giuseppe Ambrosio (2002) conducted a review in Myocardial reperfusion injury. Post-ischaemic reperfusion injury is mediated by oxygen radicals and neutrophils, leading to oxidative tissue damage, microvascular impairment, and no-reflow despite adequate epicardial flow.
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