摘要
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。
AIM： To evaluate the 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 KCI solution. Membrane patch clamp whole cell recording technique was used to investigate the Ik current maximum in the holding potential - 50 mY, lasting time 100 ms, command potential ＋ 40 mV. RESULTS： The action potential duration of 30%, 50% repolarization （APD30, APD50） and ERP were significantly prolonged, but APD90 wasn＇t prolonged significantly when captopril group compared with ischemic group. The amplitude of Ik increased significantly in ischemic group, but significantly decreased in captopril group and in captopril ＋ ischemic group. The shapes of current - voltage relationship were unchanged among groups, but significantly upward in ischemic group and downward in captopril and captopril ＋ ischemic group. CONCLUSION： Captopril exerts electrophysiologic action due to decreasing delay outward rectification potassium current and prolonging action potential duration of APD30, APD50 and ERP.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2006年第3期456-459,共4页
Chinese Journal of Pathophysiology
关键词
膜片钳术
卡托普利
动作电位
外向整流钾电流
心肌细胞
Patch - clamp techniques
Captopril
Action potentials
Outward rectifier potassium current
Myocytes
