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[心肌缺血-再灌注损伤的生化与细胞基础]

[The biochemical and cellular bases of myocardial ischemia-reperfusion damage].

作者信息

Téllez F, Carvajal K, García C, Vásquez C, Chávez E, Moreno-Sánchez R

机构信息

Departamento de Bioquímica, Instituto Nacional de Cardiología, México D.F.

出版信息

Arch Inst Cardiol Mex. 1996 Mar-Apr;66(2):162-81.

PMID:8768635
Abstract

In recent years evidence has accumulated indicating a possible myocardial injury secondary to reperfusion. However, it is not exactly known whether injury, at the time of reperfusion, merely represents an acceleration of the damage resulting from ischemia, or whether there is a specific additional injury caused by reperfusion itself. Some pathological events have been associated to reperfusion such as reperfusion arrhythmias, stunning myocardium and vascular damage with no reflow. In this review we discuss the hypotheses that explain the cellular events involved in reperfusion damage: calcium overload, free radical damage and others; also we describe both the experimental models commonly used and drugs assayed in recent years to lower the intensity of this phenomenon.

摘要

近年来,越来越多的证据表明再灌注可能会导致心肌损伤。然而,目前尚不清楚再灌注时的损伤仅仅是缺血所致损伤的加速,还是再灌注本身会造成特定的额外损伤。一些病理事件与再灌注有关,如再灌注心律失常、心肌顿抑和无复流的血管损伤。在这篇综述中,我们讨论了解释再灌注损伤中细胞事件的假说:钙超载、自由基损伤等;我们还描述了近年来常用的实验模型以及为降低这种现象的强度而检测的药物。

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Arch Inst Cardiol Mex. 1996 Mar-Apr;66(2):162-81.
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