Holubarsch C, Ruf T, Goldstein D J, Ashton R C, Nickl W, Pieske B, Pioch K, Lüdemann J, Wiesner S, Hasenfuss G, Posival H, Just H, Burkhoff D
University of Freiburg, Department of Cardiology and Angiology, Germany.
Circulation. 1996 Aug 15;94(4):683-9. doi: 10.1161/01.cir.94.4.683.
The Frank-Starling mechanism is one of the most important physiological principles for regulation of contractile performance. We therefore studied the question of whether this mechanism may be absent or attenuated in end-stage failing human left ventricular myocardium.
Different methodological approaches were used to analyze the effects of this mechanism on the organ, tissue, and sarcomere levels: (1) In excised human whole left ventricles (2 donor hearts, 5 failing hearts), diastolic and systolic pressure-volume relationships were obtained. (2) In isolated muscle strip preparations from the left ventricular wall of donor hearts (n = 14) and failing hearts from patients with idiopathic dilated cardiomyopathy (n = 21) and ischemic cardiomyopathy (n = 11), peak developed force was measured at different muscle lengths of the preparation. (3) Skinned fiber preparations were obtained from failing right and left ventricles (n = 12). In all three studies, we clearly observed the existence of the Frank-Starling mechanism: (1) In isolated failing human left ventricles, peak developed isometric pressure is increased when the preload is elevated. (2) Peak developed tension is increased by approximately 50% to 70% (P < .01) in left ventricular preparations of failing and nonfailing ventricles when the muscles are stretched from 90% to 100% optimum length. (3) An increase in sarcomere length leads to a sensitization of contractile proteins of ventricular skinned fiber preparations from failing human hearts. At 1.9-microns sarcomere length, the EC50 value was 5.56 +/- 0.06, and at 2.3 microns it was 5.70 +/- 0.05 (P < .01; n = 7).
The Frank-Starling mechanism is maintained in end-stage failing human hearts, whereas significant alterations of diastolic myocardial distensibility are evident in chronic heart failure.
Frank-Starling机制是调节收缩功能最重要的生理原理之一。因此，我们研究了该机制在终末期衰竭的人类左心室心肌中是否可能缺失或减弱的问题。
采用不同的方法来分析该机制在器官、组织和肌节水平上的作用：（1）在切除的人类完整左心室（2个供体心脏，5个衰竭心脏）中，获得舒张期和收缩期压力-容积关系。（2）在来自供体心脏左心室壁的离体肌条标本（n = 14）以及特发性扩张型心肌病患者（n = 21）和缺血性心肌病患者（n = 11）的衰竭心脏中，在标本的不同肌肉长度下测量最大收缩力。（3）从衰竭的右心室和左心室（n = 12）获取脱细胞纤维标本。在所有这三项研究中，我们都清楚地观察到了Frank-Starling机制的存在：（1）在离体的衰竭人类左心室中，当预负荷升高时，最大等长压力增加。（2）当肌肉从90%最佳长度拉伸至100%最佳长度时，衰竭和非衰竭心室的左心室标本中最大收缩张力增加约50%至70%（P <.01）。（3）肌节长度增加会导致来自衰竭人类心脏的心室脱细胞纤维标本的收缩蛋白敏感性增加。在肌节长度为1.9微米时，半数有效浓度（EC50）值为5.56±0.06，在2.3微米时为5.70±0.05（P <.01；n = 7）。
Frank-Starling机制在终末期衰竭的人类心脏中得以维持，而舒张期心肌伸展性的显著改变在慢性心力衰竭中很明显。
