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收缩蛋白在人类衰竭和非衰竭心肌中的功能。

Contractile protein function in failing and nonfailing human myocardium.

作者信息

Hasenfuss G, Mulieri L A, Leavitt B J, Allen P D, Holubarsch C, Just H, Alpert N R

机构信息

Department of Medicine, Cardiology, University of Freiburg, FRG.

出版信息

Basic Res Cardiol. 1992;87 Suppl 1:107-16. doi: 10.1007/978-3-642-72474-9_9.

DOI:10.1007/978-3-642-72474-9_9
PMID:1497566
Abstract

Isometric heat and force measurements were used to relate mechanical performance to function of contractile proteins in muscle strips from failing and nonfailing human hearts (37 degrees C, 60 beats per minute). Compared to control myocardium, crossbridge behavior was altered in myocardium from hearts with end-stage failing dilated and ischemic cardiomyopathy, resulting in increased crossbridge force-time integral by 33% and 36%, respectively. Peak isometric twitch tension was reduced significantly by 46% in muscle strips from hearts with dilated cardiomyopathy. In myocardium from hearts with ischemic cardiomyopathy peak isometric twitch tension was comparable to values from nonfailing hearts. Including all three types of myocardium, there was a close correlation between the number of crossbridge interactions during the isometric twitch (tension-dependent heat) and peak twitch tension (r = 0.88; p less than 0.001). Compared to control, in failing myocardium from dilated cardiomyopathic hearts, tension-independent heat (calcium cycling) was significantly reduced. This indicates that in dilated cardiomyopathy reduced peak twitch tension results from decreased calcium activation of contractile proteins with reduced number of crossbridge interactions during the isometric twitch. In ischemic cardiomyopathy mechanisms different from those observed in dilated cardiomyopathy seem to be involved in the development of heart failure.

摘要

采用等长热和力测量方法,将机械性能与来自衰竭和非衰竭人类心脏的心肌条中收缩蛋白的功能相关联(37摄氏度,每分钟60次心跳)。与对照心肌相比,终末期扩张型和缺血性心肌病心脏的心肌中横桥行为发生改变,导致横桥力 - 时间积分分别增加33%和36%。扩张型心肌病心脏的心肌条中,等长收缩峰值张力显著降低46%。在缺血性心肌病心脏的心肌中,等长收缩峰值张力与非衰竭心脏的值相当。纳入所有三种类型的心肌后,等长收缩期间横桥相互作用的数量(张力依赖性热)与收缩峰值张力之间存在密切相关性(r = 0.88;p < 0.001)。与对照相比,扩张型心肌病衰竭心肌中,张力非依赖性热(钙循环)显著降低。这表明在扩张型心肌病中,收缩峰值张力降低是由于等长收缩期间收缩蛋白的钙激活减少以及横桥相互作用数量减少所致。在缺血性心肌病中,心力衰竭发展似乎涉及与扩张型心肌病中观察到的机制不同的机制。

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