Hanft Laurin M, Korte Fredrick S, McDonald Kerry S
Department of Medical Pharmacology & Physiology, MA 415, Medical Sciences Building, School of Medicine, University of Missouri, Columbia, MO 65212, USA.
Cardiovasc Res. 2008 Mar 1;77(4):627-36. doi: 10.1093/cvr/cvm099. Epub 2007 Dec 12.
The Frank-Starling relationship provides beat-to-beat regulation of ventricular function by matching ventricular input and output. This review addresses the subcellular mechanisms by which the ventricle adjusts its output (i.e. stroke volume) by changes in end-diastolic volume. The subcellular processes are placed in the context of the four phases of the cardiac cycle with emphasis on the sarcomeric properties that mediate the number of force-generating cross-bridges recruited during pressure development. Additional mechanistic insight is provided regarding the factors that regulate myocyte loaded shortening speeds, which are paramount for dictating ejection volume. Emphasis is placed on the interplay between cross-bridge-induced cooperative activation of the thin filament and cooperative deactivation of the thin filament induced by muscle shortening. The balance of these two properties seems to determine systolic haemodynamics, and how this balance is modulated by sarcomere length, in part, underlies the Frank-Starling relationship.
Frank-Starling关系通过匹配心室的输入和输出实现对心室功能的逐搏调节。本综述探讨了心室通过舒张末期容积的变化来调节其输出（即每搏输出量）的亚细胞机制。这些亚细胞过程置于心动周期的四个阶段背景下，重点关注在压力产生过程中介导募集的产生力的横桥数量的肌节特性。还提供了关于调节心肌细胞加载缩短速度的因素的更多机制见解，这对于决定射血量至关重要。重点在于横桥诱导的细肌丝协同激活与肌肉缩短诱导的细肌丝协同失活之间的相互作用。这两种特性之间的平衡似乎决定了收缩期血流动力学，而这种平衡如何部分地受肌节长度调节，正是Frank-Starling关系的基础。
