Fu Yi-Cheng, Zhang Yu, Tian Liu-Yang, Li Nan, Chen Xi, Cai Zhong-Qi, Zhu Chao, Li Yang
Division of Cardiology, Chinese PLA General Hospital, Beijing, China.
J Geriatr Cardiol. 2016 May;13(4):316-25. doi: 10.11909/j.issn.1671-5411.2016.04.008.
Allocryptopine (ALL) is an effective alkaloid of Corydalis decumbens (Thunb.) Pers. Papaveraceae and has proved to be anti-arrhythmic. The purpose of our study is to investigate the effects of ALL on transmural repolarizing ionic ingredients of outward potassium current (I to) and slow delayed rectifier potassium current (I Ks).
The monophasic action potential (MAP) technique was used to record the MAP duration of the epicardium (Epi), myocardium (M) and endocardium (Endo) of the rabbit heart and the whole cell patch clamp was used to record I to and I Ks in cardiomyocytes of Epi, M and Endo layers that were isolated from rabbit ventricles.
The effects of ALL on MAP of Epi, M and Endo layers were disequilibrium. ALL could effectively reduce the transmural dispersion of repolarization (TDR) in rabbit transmural ventricular wall. ALL decreased the current densities of I to and I Ks in a voltage and concentration dependent way and narrowed the repolarizing differences among three layers. The analysis of gating kinetics showed ALL accelerated the channel activation of I to in M layers and partly inhibit the channel openings of I to in Epi, M and Endo cells. On the other hand, ALL mainly slowed channel deactivation of I Ks channel in Epi and Endo layers without affecting its activation.
Our study gives partially explanation about the mechanisms of transmural inhibition of I to and I Ks channels by ALL in rabbit myocardium. These findings provide novel perspective regarding the anti-arrhythmogenesis application of ALL in clinical settings.
别隐品碱（ALL）是罂粟科伏生紫堇中的一种有效生物碱，已被证明具有抗心律失常作用。本研究旨在探讨ALL对跨膜复极化外向钾电流（Ito）和缓慢延迟整流钾电流（IKs）离子成分的影响。
采用单相动作电位（MAP）技术记录兔心外膜（Epi）、心肌（M）和内膜（Endo）的MAP持续时间，采用全细胞膜片钳技术记录从兔心室分离的Epi、M和Endo层心肌细胞中的Ito和IKs。
ALL对Epi、M和Endo层MAP的影响不均衡。ALL可有效降低兔跨膜心室壁的复极离散度（TDR）。ALL以电压和浓度依赖性方式降低Ito和IKs的电流密度，并缩小三层之间的复极差异。门控动力学分析表明，ALL加速了M层Ito通道的激活，并部分抑制了Epi、M和Endo细胞中Ito通道的开放。另一方面，ALL主要减慢Epi和Endo层IKs通道的失活，而不影响其激活。
本研究部分解释了ALL对兔心肌Ito和IKs通道跨膜抑制的机制。这些发现为ALL在临床环境中的抗心律失常应用提供了新的视角。
