Yang B F, Du Z M, Kohei S
Department of Pharmacology, Harbin Medical University, China.
Zhongguo Yao Li Xue Bao. 1994 Jan;15(1):28-32.
Effects of flecainide (Fle) on membrane currents were studied using an isolated single atrial cell from guinea pig hearts. The tight-seal cell clamp technique was used. In the current clamp condition, Fle prolonged significantly the atrial action potential (APD) with frequency dependence. Delayed outward K+ current and outward tail current were specifically inhibited by Fle in a frequency- and concentration-dependent fashion. Fle inhibited Ik more strongly as the membrane potential became more positive from +10 mV to +60 mV. The value of Ik was attenuated to 973 pA from 1105 pA of control and the value of tail current was reduced to 113 pA from 288 pA of control at 60 mV. The drug did not affect the holding current. The effects of Fle on the action potential and transmembrane ionic currents strongly suggested that the main mechanism of action of this agent was to inhibit the voltage-dependent potassium current. In the voltage clamp condition, Fle affected neither the conventional L type Ca2+ current nor the Ik1 current significantly. Our research proved that Fle was not completely consistent with the class Ic agents, because Fle could markedly increase the APD in the experiment.
使用豚鼠心脏分离的单个心房细胞研究了氟卡尼（Fle）对膜电流的影响。采用了紧密封细胞钳技术。在电流钳制条件下，Fle显著延长心房动作电位（APD），且具有频率依赖性。延迟外向钾电流和外向尾电流受到Fle特异性抑制，呈现频率和浓度依赖性。当膜电位从+10 mV变为+60 mV时，Fle对Ik的抑制作用更强。在60 mV时，Ik值从对照的1105 pA衰减至973 pA，尾电流值从对照的288 pA降至113 pA。该药物不影响钳制电流。Fle对动作电位和跨膜离子电流的影响强烈表明，该药物的主要作用机制是抑制电压依赖性钾电流。在电压钳制条件下，Fle对传统L型钙电流和Ik1电流均无显著影响。我们的研究证明，Fle与Ic类药物并不完全一致，因为在实验中Fle可显著增加APD。
