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挥发性麻醉药心脏预处理的机制

Mechanism of cardiac preconditioning with volatile anaesthetics.

作者信息

Hu Z-Y, Liu J

机构信息

Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, PR China.

出版信息

Anaesth Intensive Care. 2009 Jul;37(4):532-8. doi: 10.1177/0310057X0903700402.

Abstract

In recent years, there has been increased interest in the mechanisms involved in anaesthetic-induced cardioprotection. It is not thoroughly understood how volatile anaesthetics protect the myocardium from ischaemia or reperfusion injury, but the overall mechanism is likely to be multifactorial. This review examines the recent experimental and clinical research underlying the cellular and molecular mechanisms involved in anaesthetic-induced preconditioning. A variety of intracellular signalling pathways have been implicated in the protective phenomenon. Ischaemic preconditioning and anaesthetic-induced preconditioning share similar molecular mechanisms, including activation of guanine nucleotide-binding proteins, triggering of second messenger pathways, activation of multiple kinases, mediation of nitric oxide formation and reactive oxygen species release, maintenance of intracellular and/or mitochondrial Ca2+ homeostasis and moderation of the opening of adenosine-triphosphate-sensitive potassium channels. A more thorough understanding of the multiple signalling steps and the ultimate cytoprotective mechanisms underlying anaesthetic-induced preconditioning may lead to improvements in the management of ischaemia and/or reperfusion injury.

摘要

近年来,人们对麻醉诱导的心脏保护机制的兴趣日益增加。目前尚不完全清楚挥发性麻醉剂如何保护心肌免受缺血或再灌注损伤,但总体机制可能是多因素的。本综述探讨了麻醉诱导预处理所涉及的细胞和分子机制的最新实验和临床研究。多种细胞内信号通路与这种保护现象有关。缺血预处理和麻醉诱导的预处理具有相似的分子机制,包括鸟嘌呤核苷酸结合蛋白的激活、第二信使途径的触发、多种激酶的激活、一氧化氮形成和活性氧释放的介导、细胞内和/或线粒体Ca2+稳态的维持以及三磷酸腺苷敏感性钾通道开放的调节。对麻醉诱导预处理背后的多个信号步骤和最终细胞保护机制有更深入的了解,可能会改善缺血和/或再灌注损伤的管理。

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