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再灌注诱导的心律失常:自由基起关键作用吗?

Reperfusion-induced arrhythmias: do free radicals play a critical role?

作者信息

Manning A S

机构信息

Department of Biology, Roché Products Limited, Welwyn Garden City, Herts, England.

出版信息

Free Radic Biol Med. 1988;4(5):305-16. doi: 10.1016/0891-5849(88)90051-2.

Abstract

This article assesses whether oxygen-derived free radicals are one of the molecular causes of life-threatening arrhythmias that arise upon reperfusion of the ischemic myocardium. Evidence supporting this proposition has been obtained from studies of the effects of free radical scavengers and antioxidants, free radical generating systems, inhibition of various sources of free radicals and studies investigating the formation of free radicals and their products during early reperfusion. It has been hypothesized that free radical formation causes localised membrane damage to the sarcolemma that results in focal alterations in transmembrane ionic fluxes, particularly potassium. These changes in ionic fluxes may then lead to electrophysiological abnormalities that culminate in ventricular arrhythmias.

摘要

本文评估氧衍生的自由基是否是缺血心肌再灌注时出现的危及生命的心律失常的分子原因之一。支持这一观点的证据来自于对自由基清除剂和抗氧化剂的作用、自由基生成系统、对各种自由基来源的抑制以及对早期再灌注期间自由基及其产物形成的研究。据推测,自由基的形成会导致肌膜局部膜损伤,从而导致跨膜离子通量,特别是钾离子通量的局部改变。离子通量的这些变化可能进而导致电生理异常,最终引发室性心律失常。

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