Kong S E, Blennerhassett L R, Heel K A, McCauley R D, Hall J C
University Department of Surgery, Royal Perth Hospital, Australia.
Aust N Z J Surg. 1998 Aug;68(8):554-61. doi: 10.1111/j.1445-2197.1998.tb02099.x.
Ischaemia-reperfusion injury (IRI) is of obvious relevance in situations where there is an interruption of blood supply to the gut, as in vascular surgery, or in the construction of free intestinal grafts. It is now appreciated that IRI also underlies the guy dysfunction that occurs in early shock, sepsis, and trauma. The events that occur during IRI are complex. However, recent advances in cellular biology have started to unravel these underlying processes. The aim of this review is to provide an outline of current knowledge on the mechanisms and consequences of IRI. Initially, IRI appears to be mediated by reactive oxygen metabolites and, at a later stage, by the priming and activation of polymorphonuclear neutrophils (PMN). Ischaemia-reperfusion injury can diminish the barrier function of the gut, and can promote an increase in the leakage of molecules (intestinal permeability) or the passage of microbes across the wall of the bowel (bacterial translocation). Ischaemia-reperfusion injury to the gut can result in the generation of molecules that may also harm distant tissues.
缺血再灌注损伤（IRI）在肠道血液供应中断的情况下具有明显的相关性，如在血管手术或游离肠移植构建中。现在人们认识到，IRI也是早期休克、脓毒症和创伤中发生的肠道功能障碍的基础。IRI期间发生的事件很复杂。然而，细胞生物学的最新进展已开始揭示这些潜在过程。本综述的目的是概述关于IRI机制和后果的当前知识。最初，IRI似乎由活性氧代谢产物介导，后期则由多形核中性粒细胞（PMN）的预激和激活介导。缺血再灌注损伤会削弱肠道的屏障功能，并可促进分子渗漏增加（肠道通透性）或微生物穿过肠壁（细菌移位）。肠道的缺血再灌注损伤可导致可能也会损害远处组织的分子生成。
