[挥发性麻醉剂对心肌的保护作用]。

Anaesthesiologie und Reanimation Pub Date : 2002-01-01
B Preckel, J Müllenheim, W Schlack
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引用次数: 0

摘要

心肌缺血/再灌注情况可能发生在围手术期。麻醉药的心脏保护作用早已为人们所知:挥发性麻醉药可减少缺血细胞损伤和梗死发展。除缺血外,再灌注本身也可导致细胞损伤,从而进一步加重缺血损伤(再灌注损伤)。吸入麻醉剂对离体心脏和兔心脏的再灌注损伤均有特殊的保护作用。这种保护不依赖于物质的血流动力学副作用,甚至在使用心脏麻痹溶液保护心脏免受缺血性损伤后也存在。短时间的缺血使心肌对随后较长时间的缺血具有抵抗力。这种针对缺血后果的最强内源性保护机制被称为缺血预处理。保护作用也可以通过刺激不同类型的受体产生:各自的激动剂产生药理学(化学)预处理。缺血和化学预处理的信号转导级联的共同途径包括肌髓和/或线粒体atp敏感的钾通道。挥发性麻醉剂可以模仿短暂缺血的保护作用,从而产生化学预处理。这种作用至少部分取决于麻醉诱导的atp敏感钾通道的打开。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Myocardial protection by volatile anesthetics].

Myocardial ischaemia/reperfusion situations may occur during the perioperative period. The cardioprotective effects of anaesthetics have been known for a long time: volatile anaesthetics reduce the ischaemic cell damage and infarct development. Besides ischaemia, reperfusion itself can also lead to cellular damage, thereby further increasing the ischaemic injury (reperfusion injury). Inhalational anaesthetics offer specific protective effects against reperfusion injury in isolated hearts as well as in rabbit hearts in vivo. This protection does not depend on haemodynamic side-effects of the substances and is even present after protecting the heart against ischaemic damage using a cardioplegic solution. Short periods of ischaemia render the myocardium resistant to subsequent longer periods of ischaemia. This strongest endogenous protective mechanism against the consequences of an ischaemia is known as ischaemic preconditioning. The protective effect can also be produced by stimulation of different types of receptors: the respective agonists produce pharmacological (chemical) preconditioning. The common pathway of the signal transduction cascade of both ischaemic and chemical preconditioning includes the sarcolemnal and/or mitochondrial ATP-sensitive potassium channel. Volatile anaesthetics can imitate the protective effects of a short ischaemia, thereby producing chemical preconditioning. This effect depends, at least in part, on anaesthetic-induced opening of ATP-sensitive potassium channels.

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