论文部分内容阅读
目的:探讨卡托普利对豚鼠心肌细胞动作电位间期及延迟整流钾电流的作用。方法:采用内充3mol/LKCl的玻璃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,保持时间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,APD90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。电流-电压关系曲线形状各组间无显著变化,缺血组显著上移而卡托普利组及卡托普利+缺血组下移。结论:卡托普利具有的电生理作用是由于它降低外向延迟整流钾电流及延长APD30、APD50和ERP。
Objective: To investigate the effect of captopril on action potential duration and delayed rectifier potassium current of guinea pig cardiomyocytes. Methods: The myocardial action potentials were recorded using a glass microelectrode filled with 3 mol / L KCl. Patch clamp whole cell technology, clamp potential-50mV, hold time 100ms, command potential +40 mV, record outward peak current delay rectifier potassium current (Ik). Results: Compared with the ischemic group, the APD30, APD50 and ERP in the captopril group were significantly prolonged, APD90 did not change significantly, the amplitude of the Ik in the ischemic group was significantly increased, and the captopril group and captopril + ischemic group were significantly decreased. There was no significant change in the shape of current-voltage curve between the groups. The ischemic group was significantly up-shifted while the captopril group and captopril + ischemic group were down-shifted. Conclusion: The electrophysiological effects of captopril are due to its reduced outward rectifier potassium current and prolonged APD30, APD50 and ERP.