关附甲素对兔心室肌晚钠电流及兴奋传导速度的影响

The effect of guanfu base A on the late sodium current and excitation conduction velocity in rabbit ventricular muscle

目的:应用微电极阵(MEA)技术研究关附甲素(GFA)对兔心室肌晚钠电流(INaL)及兴奋传导速度(ECV)的影响。方法:新西兰大白兔64只,随机分成4组:对照组(8只),GFA组(1、3、10μmol/L,每种浓度各8只),海葵毒素组(ATXⅡ,8只),ATXⅡ+GFA组(1、3、10μmol/L,每种浓度各8只)。开胸取出心脏后进行langendroff灌流,用柔性电极贴附左心室,记录各项电生理信号的变化。结果:与对照组相比,GFA 1μmol/L组、3μmol/L组、10μmol/L组心室肌场电位时限(fAPD)分别缩短至(338.88±10.93)、(327.13±11.57)、(314.25±9.38)ms(P<0.05),ECV分别减慢至(0.51±0.10)、(0.38±0.11)、(0.25±0.07)m/s(P<0.05);ATXⅡ组fAPD明显延长(P<0.05),ECV则无明显变化(P>0.05)。与ATXⅡ组相比,ATXⅡ+GFA 1μmol/L组、3μmol/L组、10μmol/L组心室肌fAPD分别缩短至(349.38±11.67)、(330.88±11.09)、(318.50±11.05)ms(P<0.05),ECV分别减慢至(0.51±0.10)、(0.41±0.08)、(0.30±0.07)m/s(P<0.05),其fAPD缩短率明显高于GFA组。结论:GFA具有抑制INaL与减缓ECV的作用,可能为其抗心律失常的主要机制。

Objective：To explore the effect of guanfu base A（GFA）on the late sodium current（INaL）and excitation conduction velocity（ECV）in rabbit ventricular muscle by Microelectrode array（MEA）technology.Method：Sixty four rabbits of either sex were randomly divided into 4groups：control group（n=8）,GFA group（1,3,and 10μmol/L,n=8for each concentration）,ATXⅡ group（n=8）,ATXⅡ＋ GFA group（1,3,and 10μmol/L,n=8for each concentration）.The heart was perfused with modified Tyrode＇s solution after removed.Flexible electrodes were attached to the left ventricle,and recorded the changes of electrophysiological signals.Result：In the GFA 1,3,and 10μmol/L groups,fAPD shortened to 338.88±10.93,327.13±11.57,and 314.25±9.38 ms,respectively（P〈0.05）,while ECV decelerated to 0.51±0.10,0.38±0.11,and 0.25±0.07m/s,respectively（P〈0.05）.In the ATXⅡ group,fAPD prolonged noticeably（P〈0.05）,however,there was no change in CV（P〈0.05）.In the ATXⅡ＋ GFA 1,3,and 10μmol/L groups,fAPD shortened to 349.38±11.67,330.88±11.09,318.50±11.05 ms,respectively（P〈0.05）,while ECV decelerated to 0.51±0.10,0.41±0.08,0.30±0.07m/s,respectively（P〈0.05）,the shortening rate in the ATX＋GFA group was significantly higher than that in the GFA group（P〈0.05）.Conclusion：GFA can inhibit INaL and decelerate ECV in rabbit ventricular muscle,and it may be the primary mechanism of its antiarrhythmic.