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Uncoupling of Muscle Shortening from Contractile Force in Intact Heart

机译:完整心脏中的肌肉缩短与收缩力的解耦

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摘要

It is well accepted that myocardial segment shortening is preceded by, and dependent upon, development of isometric force. In other words, muscle shortening is coupled in both time and amplitude to force; therefore it is assumed that dysfunctional contraction (e.g., in stunned myocardium) must be due to depressed contractility. However, it is also possible that dysfunctional shortening would result from poor coupling between force and shortening. This study was designed to test this hypothesis, and to show that it is possible to reversibly dissociate shortening from force development under certain conditions. In open-chest anesthetized dogs, 2,3-butanedione monoxime (BDM), acetylcholine and dobu-tamine were each injected directly into the left anterior descending coronary artery (LAD). The LAD was then lig-ated for 10 min to produce local myocardial ischemia, followed by reperfusion. In addition to global hemodynam-ics, regional myocardial force and segment shortening were measured in both the LAD-perfused area and that perfused by the circumflex coronary artery which served as a control area.
机译:众所周知,心肌节段缩短是在等轴测力的发展之前并取决于其发展。换句话说,肌肉缩短在时间和幅度上都与力相关。因此,假定功能障碍性收缩(例如,在震惊的心肌中)必定是由于收缩力下降所致。但是,也有可能由于力与缩短件之间的不良耦合而导致缩短件功能失调。这项研究旨在验证这一假设,并表明在某些条件下可以与力发展相反地缩短起子。在开胸麻醉的狗中,分别将2,3-丁二酮一肟(BDM),乙酰胆碱和多巴胺直接注入左冠状动脉前降支(LAD)。然后将LAD连接10分钟以产生局部心肌缺血,然后再灌注。除了总体血流动力学,还在LAD灌注区和作为控制区的回旋冠状动脉灌注区测量了局部心肌力和节段缩短。

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