Pathophysiology of ischaemia reperfusion injury: central role of the neutrophil

• Published in: British journal of surgery Vol. 78; no. 6; p. 651
• Main Authors: Welbourn, C R, Goldman, G, Paterson, I S, Valeri, C R, Shepro, D, Hechtman, H B
• Format: Journal Article
• Language: English
• Published: England 01-06-1991
• Subjects: Arachidonic Acids - metabolism; Cell Adhesion - physiology; Humans; Neutrophils - physiology; Reperfusion Injury - metabolism; Reperfusion Injury - physiopathology; Reperfusion Injury - prevention & control
• ISSN: 0007-1323
• DOI: 10.1002/bjs.1800780607

Ischaemia is a common clinical event leading to local and remote injury. Evidence indicates that tissue damage is largely caused by activated neutrophils which accumulate when the tissue is reperfused. If the area of ischaemic tissue is large, neutrophils also sequester in the lungs, inducing non-cardiogenic pulmonary oedema. Ischaemia reperfusion injury is initiated by production of reactive oxygen species which initially appear responsible for the generation of chemotactic activity for neutrophils. Later, once adherent to endothelium, neutrophils mediate damage by secretion of additional reactive oxygen species as well as proteolytic enzymes, in particular elastase. Therapeutic options for limiting ischaemia reperfusion injury include inhibition of oxygen radical formation, pharmacological prevention of neutrophil activation and chemotaxis, and also the use of monoclonal antibodies which prevent neutrophil-endothelial adhesion, a prerequisite for injury.