莲心碱对大鼠心室肌细胞I_(Na)、I_(Ca-L)及稳态外向K^+电流的影响

Effect of Liensinine on I_(Na), I_(Ca-L) and Steady-state Outward K^+ Current of Rat Ventricular Myocytes

采用膜片钳技术，研究了莲心碱（Liensinine，Lien）对大鼠心室肌细胞动作电位及钠电流（INa）、L-型钙电流（ICa－L）及稳态外向K＋电流的影响，Lien30μmol／L可显著地降低动作电位幅度、静息膜电位，延长动作电位时程。Lien10，30μmol／L分别使INa及ICa－L从给药前的（7．9±2．2）nA和（699±175）pA降至（4．3±1．7）、（1．8±1．6）nA和（203±132）、（147±121）pA。Lien10μmol／L还抑制INa、稳态外向K＋电流和ICa－L的I－V曲线并使后者的峰值电流电位略右移。提示Lien有钠、L型钙通道阻滞作用并抑制稳态外向K＋电流，这些可解释Lien广泛的抗心律失常作用机制。

Effects of Liensinine (Lien) on the action potentials, sodium channel current (INa), L-type calcium channel current (ICa-L) and steady-state outward K+ current of rat ventricular myocytes were studied by use of the whole cell recording patch clamp technique. Lien 30μmol/L could significantly reduce the action potential amplitude, resting potential and prolong the action potential duration. Lien (10 or 30μmol/L) decreased INa and ICa-L respectively from (7. 9 ± 2. 2) nA and (699± 175) pA as control level to (4. 3± 1. 7), (1. 8±1. 6 ) nA and (203±132), (147±121 ) pA. Also, Lien 10 μmol/L could inhibit the I-V curves of INa, steadystate outward K+ currents and ICa-L and slightly shift the maximum current potential of the latter to the right.The results suggested Lien has blocking actions on sodium and calcium channels and could inhibit steady-state outward K+ currents, which can explain the mechanism of extensive antiarrhythmic actions of Lien.