Ischemic post-conditioning to counteract intestinal ischemia/reperfusion injury.
Ischemic post-conditioning to counteract intestinal ischemia/reperfusion injury.
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DOI：
10.4291/wjgp.v1.i4.137
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发表时间：
2010-10-15
期刊：
影响因子：
--
通讯作者：
Montrose, Marshall H
中科院分区：
文献类型：
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作者：
Guan, Yan-Fang;Pritts, Timothy A;Montrose, Marshall H
肠缺血是一种由多种原因引起的严重疾病。再灌注是急性肠缺血治疗过程中的常见现象，但缺血/再灌注（IR）引起的损伤可能导致更严重的并发症，从肠萎缩到多器官功能衰竭和死亡。肠对IR诱导的损伤（IRI）的易感性出现在各种实验研究和临床环境中，如心脏和大血管手术以及器官移植。尽管氧自由基、白细胞活化、微血管灌注失败、细胞酸中毒和细胞内稳态紊乱已被认为是肠IRI发病机制中的重要因素，但这种疾病的潜在机制尚不清楚。到目前为止，在动物研究中，越来越多的注意力集中在预防肠IRI的潜在缺血前和缺血后治疗上，例如药物干扰IR诱导的细胞凋亡和炎症过程以及缺血预处理。然而，需要更好地了解与再灌注诱导的损伤相关的分子和细胞事件，以开发有效的临床保护方案来对抗这种疾病。在这方面，缺血后处理与实验性延长酸中毒阻断有害的再灌注作用相结合的使用可能具有特殊的临床意义。
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.