Franz Michael R, Bode Frank
Arrhythmia Service, VA Medical Center, Georgetown University Medical Center, 50 Irving Street, NW, Washington, DC 20422, USA.
Prog Biophys Mol Biol. 2003 May-Jul;82(1-3):163-74. doi: 10.1016/s0079-6107(03)00013-0.
Mechanoelectrical feedback (MEF) has become firmly established as a mechanism in which mechanical forces experienced by myocardial tissue or cell membranes convey alterations in electrophysiologic characteristics of such tissue. Observations to date mainly concern mechanically induced changes in action potential duration, resting and active potential amplitude, enhanced pacemaker frequency, or afterdepolarizations. While some of these changes (i.e. after depolarizations) may give rise to premature beats, a role of MEF in explaining sustained ventricular tachyarrhythmias has so far been elusive. Here, we review recent findings showing that acute atrial dilatation facilitates atrial fibrillation (AF) and that two stretch-activated channel (SAC) blockers (gadolinium and GsMTx-4) are able to suppress stretch-facilitated AF. These findings strongly support a role of MEF and SACs in promoting sustained arrhythmias and point to a new class of antiarrhythmic drugs.
机械电反馈（MEF）已被确认为一种机制，即心肌组织或细胞膜所经历的机械力可传递该组织电生理特性的改变。迄今为止的观察主要涉及机械诱导的动作电位持续时间、静息和动作电位幅度、起搏器频率增加或后去极化的变化。虽然其中一些变化（如后去极化）可能会引发早搏，但迄今为止，MEF在解释持续性室性心律失常方面的作用仍不明确。在此，我们回顾最近的研究发现，即急性心房扩张会促进心房颤动（AF），并且两种牵张激活通道（SAC）阻滞剂（钆和GsMTx-4）能够抑制牵张促进的AF。这些发现有力地支持了MEF和SAC在促进持续性心律失常中的作用，并指出了一类新型抗心律失常药物。
