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牵张诱导的心肌性能改变:从心室功能到细胞与分子机制

Stretch-induced modifications of myocardial performance: from ventricular function to cellular and molecular mechanisms.

作者信息

Crozatier B

机构信息

Unité INSERM U400, Faculté de Médecine, Creteil, France.

出版信息

Cardiovasc Res. 1996 Jul;32(1):25-37.

PMID:8776400
Abstract

The purpose of this review is to give an integrative view of the effect of stretch on the myocardium from ventricular function changes to cellular and molecular mechanisms. The general approach will be to discuss the cellular and molecular events which can explain the findings obtained in the whole ventricle. Following the historical development, the classical analysis of the Starling mechanism and the basis of the length-dependent process are rapidly reviewed. We then analyze in greater detail the recent findings on the mechanisms of length-dependent activation changes in contractile protein affinity for calcium, changes in intracellular calcium release, action potential changes and stretch-activated ion channels and discuss the opposite effects of stretch on ventricular contraction (mainly deactivation shortening and viscoelastic properties of the myocardium). Besides the short-term contractile response to stretch, the longer-term effects of myocardial stretch which lead to ventricular hypertrophy will be also rapidly reviewed.

摘要

本综述的目的是对拉伸对心肌的影响进行综合阐述,内容涵盖从心室功能变化到细胞及分子机制。总体方法是讨论那些能够解释在整个心室中所获发现的细胞和分子事件。按照历史发展脉络,我们将快速回顾 Starling 机制的经典分析以及长度依赖性过程的基础。接着,我们会更详细地分析近期关于收缩蛋白对钙亲和力的长度依赖性激活变化机制、细胞内钙释放变化、动作电位变化以及牵张激活离子通道的研究结果,并探讨拉伸对心室收缩的相反作用(主要是心肌的失活缩短和粘弹性特性)。除了拉伸引起的短期收缩反应外,我们还将快速回顾导致心室肥大的心肌拉伸的长期影响。

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