Katz A M
J Am Coll Cardiol. 1983 Jan;1(1):42-51. doi: 10.1016/s0735-1097(83)80009-6.
The past 25 years have seen an unprecedented growth in our understanding of the mechanisms responsible for the regulation of myocardial contractility. Beginning with a demonstration that myocardial contractility represents an important determinant of cardiac function, this quarter century has witnessed a series of attempts to explain length-independent changes in myocardial contractile function. Alterations in the properties of the cardiac contractile proteins and changes in the amount of calcium (Ca2+) available for binding to the contractile proteins during excitation-contraction coupling are now recognized as important biochemical bases for physiologic, pharmacologic and pathologic changes in myocardial contractility. Identification of the central role of Ca2+ in the initiation of the cardiac contractile process has made possible the analysis of the mechanisms by which several drugs alter myocardial contractile function, including the biochemical processes that allow beta-adrenergic agonists to enhance contractility. The rapid developments in this field since 1958 promise an even greater flow of new knowledge regarding the causes, prevention and treatment of heart failure provided that there is given adequate support for such research activities.
在过去25年里，我们对心肌收缩力调节机制的理解有了前所未有的增长。从证明心肌收缩力是心脏功能的一个重要决定因素开始，在这四分之一世纪里见证了一系列解释心肌收缩功能长度非依赖性变化的尝试。心肌收缩蛋白特性的改变以及在兴奋 - 收缩偶联过程中可用于与收缩蛋白结合的钙（Ca2+）量的变化，现在被认为是心肌收缩力生理、药理和病理变化的重要生化基础。Ca2+在心脏收缩过程起始中的核心作用的确定，使得分析几种药物改变心肌收缩功能的机制成为可能，包括使β - 肾上腺素能激动剂增强收缩力的生化过程。自1958年以来该领域的快速发展预示着，只要为这类研究活动提供足够的支持，将会有更多关于心力衰竭病因、预防和治疗的新知识涌现。
