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远隔预处理:内皮血管活性物质在缺血再灌注损伤心脏保护中的作用。

Preconditioning at a distance: Involvement of endothelial vasoactive substances in cardioprotection against ischemia-reperfusion injury.

机构信息

Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala 147002, India.

Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala 147002, India.

出版信息

Life Sci. 2016 Apr 15;151:250-258. doi: 10.1016/j.lfs.2016.03.021. Epub 2016 Mar 12.

DOI:10.1016/j.lfs.2016.03.021
PMID:26979771
Abstract

There is growing preclinical as well as clinical evidence supporting remote ischemic preconditioning (RIPC), in which short cycles of non-fatal ischemia followed by reperfusion to an organ or tissue distant from the heart elicits cardioprotection. It is the most practical, non-invasive, cost-free, and clinically compatible, secure procedure for reducing ischemia-reperfusion induced injury. The use of a conventional blood pressure cuff on the upper or lower limb in eliciting cardioprotection has expedited its clinical applicability. Endothelium has been documented to respond very quickly to blood flow and hypoxia by releasing different humoral factors such as endothelium derived releasing factor, endothelium derived contracting factor, endothelium derived hyperpolarizing factor. In recent years, there have been studies suggesting the key role of endothelial derived factors in RIPC induced cardioprotection. The signaling cascade involves nitric oxide, gap junctions, epoxyeicosatrienoic (EETs) acids, Ca-activated K(+) channels, angiotensin II, thromboxane A2, superoxide anions and prostacyclin. The present review describes the role of these endothelial derived factors in RIPC induced cardioprotection with possible mechanisms.

摘要

越来越多的临床前和临床证据支持远程缺血预处理(RIPC),即通过对远离心脏的器官或组织进行短暂的非致命性缺血再灌注循环,引发心脏保护作用。这是一种最实用、非侵入性、免费、与临床兼容、安全的方法,可减少缺血再灌注引起的损伤。使用传统血压袖带在上肢或下肢诱发心脏保护作用,加快了其临床应用。已有研究证实,内皮细胞对血流和缺氧的反应非常迅速,会释放不同的体液因子,如内皮衍生释放因子、内皮衍生收缩因子、内皮衍生超极化因子。近年来,有研究表明内皮衍生因子在 RIPC 诱导的心脏保护中起关键作用。信号级联反应涉及一氧化氮、缝隙连接、环氧二十碳三烯酸(EETs)酸、Ca 激活的 K(+)通道、血管紧张素 II、血栓素 A2、超氧阴离子和前列环素。本文综述了这些内皮衍生因子在 RIPC 诱导的心脏保护中的作用及其可能的机制。

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