哇巴因和乌头碱对豚鼠和大鼠心肌细胞钠电流的作用  

Effects of ouabain and aconitine on sodium currents of isolated guinea pig and rat ventricular myocytes

作　　者：龚冬梅[1] 邹晓龙[2] 白云龙[1] 单璐琛[1] 孟庆新[3] 于金玲[1] 王绍婷[1] 吕延杰[1] 杨宝峰[1] 

机构地区：[1]哈尔滨医科大学药理学教研室,黑龙江哈尔滨150081 [2]哈尔滨医科大学第一临床医学院普外科,黑龙江哈尔滨150001 [3]哈尔滨医科大学第二临床医学院心外科,黑龙江哈尔滨150081

出　　处：《哈尔滨医科大学学报》2006年第5期347-350,共4页Journal of Harbin Medical University

基　　金：国家自然科学基金资助项目(30572181);黑龙江省教育厅资助项目(11511231)

摘　　要：目的观察哇巴因和乌头碱对豚鼠和大鼠心肌细胞钠电流的作用,探讨二药诱发心律失常的机制。方法用全细胞膜片钳技术分别记录豚鼠和大鼠单个心肌细胞钠电流。结果在-40mV电压下,哇巴因5μmol/L使INa从(-48.3±8.9)pA/pF减少到(-22.6±5.6)pA/pF(抑制60.1%,n=5,P<0.01);乌头碱1μmol/L使INa从(-21.8±5.8)pA/pF增加到(-67.3±7.8)pA/pF(增加208.7%,n=4,P<0.01)。结论哇巴因抑制豚鼠心肌细胞钠电流而乌头碱增加大鼠心肌细胞钠电流。不论是抑制还是促进钠电流,二药均使离子通道失衡,这是其诱发心律失常的重要机制。Objective To observe the effects of ouabain and aconitine on INa of isolated guinea pig and rat ventricular myocytes. To discuss the arrhythmic mechanisms of the two drugs. Methods Whole cell patch clamp mode was used to record sodium current of isolated single ventricular myocytes. Results 5μmol/L ouabain inhibited INa from （ -48.3±8.9 ） pA/pF to （ -22.6±5.6） pA/pF at -40mV （inhibition rate of 60.1%,n=5,P〈0.01 ）. 1μmol/L aconitine increased INa from （ -21.8 ± 5.8）pA/pF to （-67.3±7.8） pA/pF at -40mV（increase rate of 208.7%,n =4, P 〈 0.01）.Conclusion Ouabain can decrease sodium current and aconitine can increase sodium current. Either decrease or increase of INa, these two drugs could destroy the balance of ion channels in the heart which is the important mechanism of arrhythmia.

关 键 词：哇巴因 乌头碱 INa 心律失常 膜片钳 

分 类 号：R965[医药卫生—药理学]