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Myocardial reperfusion injury

G. Ambrosio* and I. Tritto

Division of Cardiology, University of Perugia School of Medicine, Perugia, Italy

* Correspondence: Giuseppe Ambrosio, MD, PhD, Division of Cardiology, University of Perugia, Policlinico Monteluce, Via Brunamonti, Perugia, Italy.

Abstract

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.

Key Words: Myocardial ischemia • neutrophils • no-reflow • oxidant stress • reperfusion injury


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