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心肌收缩力调节中的“紧张性”和“相性”机制。

"Tonic" and "phasic" mechanisms in the regulation of myocardial contractility.

作者信息

Katz A M

出版信息

Basic Res Cardiol. 1976 Sep-Oct;71(5):447-55. doi: 10.1007/BF01909761.

Abstract

Myocardial contractility can be regulated by two types of control mechanism. A "tonic control mechanism", which allows the heart to respond to sustained changes in circulatory dynamics, appears to operate through changes in the structure of various constituents of the myocardium, best understood of these being changes in the myosin molecule that cause alterations in both myosin ATPase activity and contractility. Beat-to-beat changes in myocardial contractility are affected by a "phasic control mechanism" that involves changes in at least five calcium fluxes in the myocardium. The effects of catecholamines, many of which appear to be mediated by cyclic AMP, can be understood in terms of the modification of several of the calcium fluxes involved in the phasic control of myocardial contractility.

摘要

心肌收缩力可通过两种控制机制进行调节。一种是“紧张性控制机制”,它使心脏能够对循环动力学的持续变化做出反应,其作用似乎是通过心肌各种成分结构的改变来实现的,其中最容易理解的是肌球蛋白分子的变化,这种变化会导致肌球蛋白ATP酶活性和收缩力的改变。心肌收缩力逐搏的变化受“相位控制机制”影响,该机制涉及心肌中至少五种钙通量的变化。儿茶酚胺的作用,其中许多似乎是由环磷酸腺苷介导的,可以从参与心肌收缩力相位控制的几种钙通量的改变方面来理解。

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