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Ischaemia-reperfusion injury 

Ischaemia-reperfusion injury
Ischaemia-reperfusion injury

David A. Russell

, Nadeem A. Mughal

, and Shervanthi Homer-Vanniasinkam

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date: 07 July 2020

Tissue hypoxia from any cause leads to a series of metabolic and structural changes within cells and the extracellular milieu, which promote cellular injury and initiation of a sterile inflammatory response. Reperfusion can accentuate these responses with shifts in the redox balance, activation and recruitment of inflammatory cells, endothelial cell and microcirculatory dysfunction all exacerbating the initial injury. This ischaemia-reperfusion injury (IRI) can be induced by any condition causing generalized or single organ hypoxia including sleep apnoea, sickle cell disease, shock, single organ (myocardium, kidney, brain), or limb ischaemia and organ transplantation. The response to IRI is organ specific, may be local or systemic (systemic inflammatory response syndrome (SIRS)), and differs in warm versus cold ischaemia. This chapter will describe the underlying pathophysiology of IRI and the clinical manifestations relevant to vascular surgery, and identify potential therapeutic strategies subject to ongoing research and clinical trials.

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