Imanishi S, Arita M
Department of Physiology, Kanazawa Medical University.
Nihon Rinsho. 1993 May;51(5):1203-9.
Contraction-excitation feedback is defined as a change in the mechanical state that precedes or alters the transmembrane electrical potential. The latter could be an important electrophysiologic disorder in patients with cardiac failure since the electrophysiological changes may be induced by alterations in ventricular size, pressure or factors common to all types of congestive heart failure, regardless of aetiology. A stretch of the ventricular myocardium caused (1) a shortening of the action potential duration (APD), (2) a decrease in the resting potential (RP) and (3) the early or delayed after-depolarization that culminated in the triggered activity. Failing myocardium without ventricular hypertrophy also showed (1) a reduction in the RP and the action potential upstroke velocity and (2) APD shortening. In contrast, the majority of investigators have found a significant lengthening of the APD in the hypertrophied myocardium. These electrophysiologic changes shown in the failing myocardium with or without hypertrophy and in the mechanically stretched myocardium may be a possible substrate for the genesis of the reentrant circuit and the early or delayed afterdepolarizations, leading to ventricular arrhythmia.
收缩 - 兴奋反馈被定义为在跨膜电位之前或改变跨膜电位的机械状态变化。后者可能是心力衰竭患者的一种重要电生理紊乱,因为电生理变化可能由心室大小、压力的改变或所有类型充血性心力衰竭共有的因素引起,而与病因无关。心室心肌的拉伸导致(1)动作电位持续时间(APD)缩短,(2)静息电位(RP)降低,以及(3)早期或延迟后去极化,最终导致触发活动。无心室肥厚的衰竭心肌也表现出(1)RP和动作电位上升速度降低,以及(2)APD缩短。相比之下,大多数研究者发现肥厚心肌中的APD显著延长。在有或无肥厚的衰竭心肌以及机械拉伸的心肌中显示的这些电生理变化可能是折返环路以及早期或延迟后去极化发生的可能基础,从而导致室性心律失常。