青藤碱对豚鼠心室肌细胞膜钾离子通道的阻滞作用

The Inhibition of Sinomenine on Inward Rectifier Potassium Current and Delayed Rectifying Potassium Current in Isolated Guinea Pig Ventricular Myocyte Membrane

利用膜片钳全细胞记录技术研究青藤碱（Ｓｉｎ）对分离的豚鼠单个心室肌细胞膜内向整流钾电流（Ｉｋ１）和延迟整流钾电流（ＩＫ）的影响，发现１μｍｏｌ／Ｌ和５μｍｏｌ／Ｌ的Ｓｉｎ使ＩＫｍａｘ（去极化终末最大ＩＫ）从３５５．９±２１．９ｐＡ分别降至３１７．６±２０．１ｐＡ和２３３．１±１８．７ｐＡ（ｎ＝７，Ｐ均＜０．０５），分别降低了１０．８％和３４．４％；外向尾电流从１５５．１±９．３ｐＡ分别降至１２９．４±６．２ｐＡ和９１．８±６．９ｐＡ（ｎ＝７，Ｐ均＜０．０５），分别降低了１６．６％和４０．８％。当维持电压－４０ｍＶ，超极化－１００ｍＶ时，１μｍｏｌ／Ｌ和５μｍｏｌ／Ｌ的Ｓｉｎ使Ｉｋ１从３．１５７±０．７９４ｎＡ分别降至２．７３５±０．７９９ｎＡ和２．４１１±０．５８１ｎＡ（ｎ＝８，Ｐ均＜０．０１），抑制率分别为１３．４％和２３．６％。５μｍｏｌ／ＬＳｉｎ于不同膜电位水平均能抑制Ｉｋ１，且使Ｉｋ１Ｉ－Ｖ曲线零电位从－８０ｍＶ降至－７０ｍＶ。结果表明Ｓｉｎ对ＩＫ和Ｉｋ１均具浓度依赖性阻滞作用，其延长心肌细胞的复极效应可能与钾通道阻滞有关。

Patch clamp technique was used to investigate the effect of sinomenine(Sin) on inward rectifier potassium current (I k1 ) and delayed rectifying potassium current (IK) in isolated guinea pig ventricular myocyte membrane.1,5 μmol/L Sin decreased IKmax from 355.9±21.9 pA to 317.6±20.1 pA (10.8%) and 233.1±18.7 pA(34.4%) respectively ( n =7, P <0.05),IKtail from 155.1±9.3 pA to 129.4±6.2 pA(16.6%) and 91.8±6.9 pA (40.8%) respectively ( n =7, P <0.05).When holding potential was -40 mV,command potential was -100 mV,1,5 μmol/L Sin also inhibited I k1 from 3.157±0.794 nA to 2.735±0.799 nA(13.4%) and 2.411±0.581 nA (23.6%) respectively ( n =8, P <0.01),5 μmol/L Sin blocked I k1 at all membrane potentials and changed the reverse potential of I V curve from -80 mV to -70 mV.These results indicate that Sin blocks IK and I k1 in a concentration dependent manner and results in the lengthen of action potential duration (APD) in cardiac myocytes.