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持久的心脏过强活动常导致心肌收缩力的减弱。长期血流动力负荷过重时,心肌消耗的能量增加,而心肌产生的能量是有限的,故重建产能与耗能的平衡就成为代偿机理的一部分。所以心肌对慢性负荷过重的反应是增加心脏搏血能力与压抑心脏活动以节约能量。 心肌在功能上是合体细胞,心脏的收缩活动不能像骨骼肌一样由神经系统兴奋的运动单位的数量来调节。心肌活动所能调节的是每个心肌细胞的活动强度,即受细胞内生物化学与生物理性调节。本文着重讨论细胞内引起收缩过程的蛋白质和调节收缩强度的膜性结构。
Long-lasting cardiac activity often leads to myocardial contractility weakened. Long-term hemodynamic overload, the energy consumed by the myocardium increases, and the energy generated by the myocardium is limited, so the balance between rebuilding capacity and energy consumption has become part of the compensatory mechanism. Therefore, the reaction of myocardium to chronic overload is to increase the ability to beat the heart and suppress heart activity to save energy. Cardiac muscle is functionally a syncytial cell, and cardiac contractile activity can not be regulated by the number of motor units excited by the nervous system like skeletal muscle. Myocardial activity can regulate the activity of each cardiomyocyte activity, that is, by intracellular biochemistry and biophysical regulation. This article focuses on the proteins that cause contraction in the cell and the membranous structure that regulates the strength of contraction.