Liu T F, Chen X J
Department of Biology, Peking University, Beijing, China.
Methods Find Exp Clin Pharmacol. 1993 Mar;15(2):71-5.
The effects of pinacidil and acetylcholine (Ach) on action potential (AP) and early afterdepolarization (EAD) were investigated in mouse atrial fibers. Under treatment with pinacidil the AP and EAD were affected only with the concentration of 8 x 10(-5) M, which inhibited EAD but did not affect AP except for only a minor reduction of action potential duration (APD). After withdrawal of pinacidil, the inhibitory effect of EAD was enhanced. Under treatment with Ach (2 x 10(-7) M), AP was not changed except the APD, which was significantly reduced, and the EAD was completely abolished. Withdrawal of Ach produced a rebound increase in APD and led to induction of EAD or promoted EAD to more extensive level such as appearance of long second plateau. Atropine (1 x 10(-7) M) abolished the rebound effect caused by withdrawal of Ach. The mechanism of EAD generation induced by removing Ach is discussed.
在小鼠心房纤维中研究了吡那地尔和乙酰胆碱(Ach)对动作电位(AP)和早期后除极(EAD)的影响。在用吡那地尔治疗时,仅在浓度为8×10⁻⁵ M时AP和EAD受到影响,该浓度抑制EAD,但除动作电位时程(APD)略有缩短外不影响AP。停用吡那地尔后,EAD的抑制作用增强。在用Ach(2×10⁻⁷ M)治疗时,除APD显著缩短外AP无变化,且EAD完全消失。停用Ach导致APD反跳性增加,并导致EAD的诱导或使EAD发展到更广泛的程度,如出现长的第二个平台期。阿托品(1×10⁻⁷ M)消除了停用Ach引起的反跳效应。讨论了去除Ach诱导EAD产生的机制。