Department of Physiology, Wayne State University, Rm 4126 Scott Hall, 540 E Canfield, Detroit, MI, 48201, USA.
Arch Biochem Biophys. 2019 Mar 30;664:62-67. doi: 10.1016/j.abb.2019.01.034. Epub 2019 Jan 30.
Movement of the myocardium can modify organ-level cardiac function and its molecular (crossbridge) mechanisms. This motion, which is defined by myocardial strain and strain rate (muscle shortening, lengthening, and the speed of these movements), occurs throughout the cardiac cycle, including during isovolumic periods. This review highlights how the left ventricular myocardium moves throughout the cardiac cycle, how muscle mechanics experiments provide insight into the regulation of forces used to move blood in and out of the left ventricle, and its impact on (and regulation by) crossbridge and sarcomere kinetics. We specifically highlight how muscle mechanics experiments explain how myocardial relaxation is accelerated by lengthening (strain rate) during late systole and isovolumic relaxation, a lengthening which has been measured in human hearts. Advancing and refining both in vivo measurement and ex vivo protocols with physiologic strain and strain rates could reveal important insights into molecular (crossbridge) kinetics. These advances could provide an improvement in both diagnosis and precise treatment of cardiac dysfunction.
心肌运动可以改变器官水平的心脏功能及其分子（横桥）机制。这种运动通过心肌应变和应变速率（肌肉缩短、拉长和这些运动的速度）来定义，发生在整个心动周期内，包括等容期。本综述重点介绍了左心室心肌在心动周期中的运动方式、肌肉力学实验如何深入了解用于将血液进出左心室的力的调节，以及其对（和由）横桥和肌节动力学的影响。我们特别强调了肌肉力学实验如何解释心肌舒张如何通过收缩末期和等容舒张期的拉长（应变率）加速，在人类心脏中已经测量到这种拉长。推进和完善具有生理应变和应变率的体内测量和离体方案，可以深入了解分子（横桥）动力学。这些进展可以提高心脏功能障碍的诊断和精确治疗水平。
