Published online 19 October 2004
British Medical Bulletin, Vol. 70 © The British Council 2004; all rights reserved
Vascular ischaemia and reperfusion injury
* Department of Anesthesiology and Intensive Care Medicine, University Hospital, Tübingen, Germany and Department of Cardiovascular Anesthesia, Texas Heart Institute, Saint Luke’s Episcopal Hospital, Houston, TX 77030, USA
Correspondence to: Charles D. Collard, Clinical Associate Professor, Department of Cardiovascular Anesthesia, Texas Heart Institute, St. Luke’s Episcopal Hospital, 6720 Bertner Avenue, Room 0520, MC1-226, Houston, TX 77030, USA. E-mail: ccollard{at}heart.thi.tmc.edu
Although restoration of blood flow to an ischaemic organ is essential to prevent irreversible tissue injury, reperfusion per se may result in a local and systemic inflammatory response that may augment tissue injury in excess of that produced by ischaemia alone. Cellular damage after reperfusion of previously viable ischaemic tissues is defined as ischaemia–reperfusion (I–R) injury. I–R injury is characterized by oxidant production, complement activation, leucocyte–endothelial cell adhesion, platelet–leucocyte aggregation, increased microvascular permeability and decreased endothelium-dependent relaxation. In its severest form, I–R injury can lead to multiorgan dysfunction or death. Although our understanding of the pathophysiology of I–R injury has advanced significantly in the last decade, such experimentally derived concepts have yet to be fully integrated into clinical practice. Treatment of I–R injury is also confounded by the fact that inhibition of I–R-associated inflammation might disrupt protective physiological responses or result in immunosuppression. Thus, while timely reperfusion of the ischaemic area at risk remains the cornerstone of clinical practice, therapeutic strategies such as ischaemic preconditioning, controlled reperfusion, and anti-oxidant, complement or neutrophil therapy may significantly prevent or limit I–R-induced injury in humans.
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