Post-ischaemic organ dysfunction: a review.
OBJECTIVE
The aim of this review is to consider the pathophysiology of ischaemia-reperfusion in organs that may be affected by either its local or remote consequences. Potential therapeutic strategies are also considered.


METHODS
A general discussion of the biochemical (including oxygen free radicals, complement, cytokines) and cellular events (endothelial cells, neutrophils) responsible for the mediation of reperfusion injury is presented, with special consideration of the organ-specific differences affecting the myocardium, central nervous system, gut, liver, kidney and skeletal muscle. Similarly, events which promote remote organ injury are described.


CONCLUSIONS
Although it is recognised that prolonged ischaemia results in tissue and organ damage, the concept of reperfusion-induced tissue injury, defined as tissue damage occurring as a direct consequence of revascularisation, is relatively recent. Such events may increase the morbidity and mortality of patients undergoing vascular reconstruction, trauma surgery and transplantation. A clear understanding of the factors responsible for its development is therefore vital if protocols that reduce its impact are to be developed.
Homer-Vanniasinkam
S
S
Vascular Surgical Unit, General Infirmary at Leeds, U.K.
Crinnion
J N
JN
Gough
M J
MJ
D000818:Animals; D006801:Humans; D015427:Reperfusion Injury / Q000209:etiology / Q000503:physiopathology