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缺血后处理对抗肠道缺血/再灌注损伤。

Ischemic post-conditioning to counteract intestinal ischemia/reperfusion injury.

作者信息

Guan Yan-Fang, Pritts Timothy A, Montrose Marshall H

机构信息

Yan-Fang Guan, Marshall H Montrose, Department of Molecular and Cellular Physiology, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267, United States.

出版信息

World J Gastrointest Pathophysiol. 2010 Oct 15;1(4):137-43. doi: 10.4291/wjgp.v1.i4.137.

DOI:10.4291/wjgp.v1.i4.137
PMID:21607154
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3097957/
Abstract

Intestinal ischemia is a severe disorder with a variety of causes. Reperfusion is a common occurrence during treatment of acute intestinal ischemia but the injury resulting from ischemia/reperfusion (IR) may lead to even more serious complications from intestinal atrophy to multiple organ failure and death. The susceptibility of the intestine to IR-induced injury (IRI) appears from various experimental studies and clinical settings such as cardiac and major vascular surgery and organ transplantation. Whereas oxygen free radicals, activation of leukocytes, failure of microvascular perfusion, cellular acidosis and disturbance of intracellular homeostasis have been implicated as important factors in the pathogenesis of intestinal IRI, the mechanisms underlying this disorder are not well known. To date, increasing attention is being paid in animal studies to potential pre- and post-ischemia treatments that protect against intestinal IRI such as drug interference with IR-induced apoptosis and inflammation processes and ischemic pre-conditioning. However, better insight is needed into the molecular and cellular events associated with reperfusion-induced damage to develop effective clinical protection protocols to combat this disorder. In this respect, the use of ischemic post-conditioning in combination with experimentally prolonged acidosis blocking deleterious reperfusion actions may turn out to have particular clinical relevance.

摘要

肠缺血是一种病因多样的严重病症。再灌注是急性肠缺血治疗过程中的常见情况,但缺血/再灌注(IR)所致损伤可能会引发更严重的并发症,从肠萎缩到多器官功能衰竭甚至死亡。从各种实验研究以及心脏和大血管手术、器官移植等临床情况来看,肠道对IR诱导损伤(IRI)的易感性较为明显。虽然氧自由基、白细胞活化、微血管灌注衰竭、细胞酸中毒以及细胞内稳态紊乱被认为是肠IRI发病机制中的重要因素,但该病症的潜在机制尚不明确。迄今为止,动物研究越来越关注可能的缺血前后治疗方法,这些方法可预防肠IRI,如药物干预IR诱导的凋亡和炎症过程以及缺血预处理。然而,需要更深入了解与再灌注诱导损伤相关的分子和细胞事件,以制定有效的临床保护方案来对抗这种病症。在这方面,将缺血后处理与实验性延长酸中毒相结合以阻断有害的再灌注作用,可能具有特殊的临床意义。

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本文引用的文献

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The multidimensional physiological responses to postconditioning.多维度的生理反应对后处理。
Antioxid Redox Signal. 2011 Mar 1;14(5):791-810. doi: 10.1089/ars.2010.3396. Epub 2010 Nov 2.
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Toll-like receptors: a novel target for therapeutic intervention in intestinal and hepatic ischemia-reperfusion injury? Toll 样受体:治疗肠和肝缺血再灌注损伤的新靶点?
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Ischemic postconditioning does not attenuate ischemia-reperfusion injury of rabbit small intestine.缺血后处理不能减轻兔小肠缺血再灌注损伤。
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Proteomics of ischemia/reperfusion injury in rat intestine with and without ischemic postconditioning.缺血/再灌注损伤大鼠肠组织蛋白质组学研究及其缺血后适应的作用。
J Surg Res. 2010 Nov;164(1):e173-80. doi: 10.1016/j.jss.2009.10.003. Epub 2009 Oct 24.
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Cardiac effects of postconditioning depend critically on the duration of reperfusion and reocclusion episodes.
Heart Surg Forum. 2010 Feb;13(1):E52-6. doi: 10.1532/HSF98.20091135.
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Peptides targeting Toll-like receptor signalling pathways for novel immune therapeutics.针对 Toll 样受体信号通路的肽类新型免疫治疗药物。
Curr Pharm Des. 2010;16(9):1063-80. doi: 10.2174/138161210790963841.
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Neuroprotection against spinal cord ischemia-reperfusion injury induced by different ischemic postconditioning methods: roles of phosphatidylinositol 3-kinase-Akt and extracellular signal-regulated kinase.不同缺血后处理方法诱导的脊髓缺血再灌注损伤的神经保护作用:磷脂酰肌醇3激酶-蛋白激酶B和细胞外信号调节激酶的作用
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