Sonnenblick E H
Cardiovascular Unit, Peter Bent Brigham Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Circulation. 1968 Jul;38(1):29-44. doi: 10.1161/01.cir.38.1.29.
The electron microscopic structure of heart muscle and the ultrastructural basis of cardiac contraction have been reviewed. The relation between muscle length and developed tension has been explained in terms of the structure of the sarcomere, which is the basic unit of contraction. Using the derived length-tension curve of the sarcomere, developed tension has been attributed to the overlap of thick and thin filaments within the sarcomere, lending support to the "sliding" mechanism in heart muscle. It has been shown that initial sarcomere length is a function of ventricular filling pressure and that this relation explains the normal limits of the heart as a pump, including: (1) the Starling mechanism whereby increased diastolic volume (EDV) engenders an increased stroke volume (SV), (2) the upper limits to ventricular filling pressure and volume, and (3) the normal range to the ventricular ejection fraction (SV/EDV). Further, ultrastructure helps to define the processes which occur with acute and chronic ventricular dilatation. In this regard, the importance of sarcomere dispersion and "fiber slippage," which may lead to disordered ventricular function, have been discussed.
本文综述了心肌的电子显微镜结构以及心脏收缩的超微结构基础。肌肉长度与产生的张力之间的关系已根据肌节(收缩的基本单位)的结构进行了解释。利用推导得出的肌节长度-张力曲线,产生的张力归因于肌节内粗、细肌丝的重叠,这为心肌的“滑动”机制提供了支持。研究表明,初始肌节长度是心室充盈压的函数,并且这种关系解释了心脏作为泵的正常限度,包括:(1)Starling机制,即舒张末期容积(EDV)增加会导致每搏输出量(SV)增加;(2)心室充盈压和容积的上限;(3)心室射血分数(SV/EDV)的正常范围。此外,超微结构有助于确定急性和慢性心室扩张时发生的过程。在这方面,已经讨论了可能导致心室功能紊乱的肌节离散和“纤维滑动”的重要性。