卡托普利对豚鼠心室肌细胞动作电位及外向延迟整流钾电流的作用

目的 探讨卡托普利对豚鼠心室肌细胞动作电位及外向延迟整流钾电流的作用。方法 采用内充3M KCL的标准微电极记录心肌动作电位。采用膜片钳全细胞技术，钳制电位-50mV，持续时间100ms，指令电位 40mV，记录外向延迟整流钾电流(Ik)最大峰电流。结果 与缺血组比较，卡托普利组APD30、APD50及ERP显著延长，APD50无显著变化。缺血组Ik幅度显著增高，而卡托普利组及卡托普利 缺血组显著降低。各组电流—电压关系曲线形态虽无显著变化，但缺血组显著上移，而卡托普利组、卡托普利 缺血组比缺血组下移。结论卡托普利降低外向钾电流及延长APD30、APD50和ERP。

Effect of Captopril on prolongation of action potential duration and outward delayed rectification potassium current of in guinea pig ventricular myocytes

Objective To evaluate effect of Captopril on action potential duration and outward delayed rectification potassium current(Ik).Methods Action potentials were recorded using a conventional glass microelectrode filled with 3 mol/L KCl solution.Membrane patch clamp whole cell recording technique was used to investigate Ik current maximum in holding potential -50 mV,lasting time 100ms,command potential 40 mV.Results In Captopril group, action potential duration of 30%,50% repolarization (APD30,APD50)and ERP significantly prolonged,but APD90 did not prolong significantly compared with ischemic group.Amplitude of Ik increased significantly in ischemic group, but significantly decreased in captopril group and in captopril ischemic group.Shape of current -voltage relationship curve was unchanged among groups,but significantly upward in ischemic group and downward in captopril and captopril ischemic group.Conclusion Captopril could decrease delay outward rectification potassium current and prolong action potential duration of APD30, APD50 and ERP. [