Journal Article

Myocardial reperfusion injury

G. Ambrosio and I. Tritto

in European Heart Journal Supplements

Published on behalf of European Society of Cardiology

Volume 4, issue suppl_B, pages B28-B30
Published in print March 2002 | ISSN: 1520-765X
Published online March 2002 | e-ISSN: 1554-2815 | DOI:
Myocardial reperfusion injury

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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.

Keywords: Myocardial ischemia; neutrophils; no-reflow; oxidant stress; reperfusion injury

Journal Article.  0 words. 

Subjects: Cardiovascular Medicine

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