Narimatsu E, Iwasaki H, Namiki A
Department of Anesthesiology, Sapporo Medical University, School of Medicine.
Masui. 1994 Oct;43(10):1446-53.
The classical view of the neuromuscular transmission is that non-depolarizing muscle relaxants (MRs) enhance run-down of the endplate potentials (epps) by blocking pre-junctional nicotinic acetylcholine (ACh) receptors. Several recent investigations, when extended to pharmacology, have provided evidence to suggest the existence of other types of enhancement of run-down of epps by MRs; the enhancement of epps occurs without reduction of ACh release in the presence of MRs. It has been generally accepted that the enhancement of run-down of epps causes the tetanic fade of tension response. However, recent evidence indicates that run-down of epps does not always cause this wane in tension. The electrophysiological mechanism of run-down of epps at the neuromuscular junction and the relationship between that phenomenon and the extent of reduction of tension response are described based on a review of literature and our current investigations.
神经肌肉传递的经典观点认为,非去极化肌肉松弛剂(MRs)通过阻断突触前烟碱型乙酰胆碱(ACh)受体来增强终板电位(epps)的衰减。最近的一些研究扩展到药理学领域,提供了证据表明MRs存在其他增强epps衰减的类型;在存在MRs的情况下,epps的增强发生在不减少ACh释放的情况下。人们普遍认为,epps衰减的增强会导致强直收缩张力反应的减弱。然而,最近的证据表明,epps的衰减并不总是导致这种张力减弱。基于文献综述和我们目前的研究,描述了神经肌肉接头处epps衰减的电生理机制以及该现象与张力反应降低程度之间的关系。