【摘要】 目的:研究雌二醇（Estradiol,Est）对心室肌细胞动作电位（AP）、内向整流钾通道电流(I_K1)及延迟整流钾通道电流（I_K）的影响。方法:全细胞膜片箝技术。结果:EST 10μmol·L^-1使豚鼠心室肌细胞AP时程明显缩短,APD₅₀由给药前（474±71）ms缩短至（330±75）ms（P<0.05）,Est 100μmol·L^-1使APD₅₀缩短至（229±67）ms（P<0.01）,使APD₉₀由（587±60）ms缩短至（418±79）ms（P<0.05）。Est浓度依赖性地抑制I_K尾电流（I_K·tail）,10μmol·L^-1浓度下,I_K·tail减少53％（P<0.05）,100μmol·L^-1浓度下,I_K·tail减少80％（P<0.05）。10μmol·L^-1以上浓度Est明显抑制I_K1,在-100mV刺激电压下,内向电流最大抑制为49％（P<0.01）;在-40mV刺激电压下,外向电流最大抑制为72％（P<0.01）。同时,Est使I_K1翻转电位向负电位方向移位（由-70mV变为-76mV）。结论:Est对豚鼠心室肌细胞I_K1和I_K通道具有明显的抑制作用。更多还原

【Abstract】 AIM: To study the effects of estradiol (Est) on inward rectifier K+ ( IKl) and delayed rectifier K+ ( IK) channels in isolated guinea pig ventricular myocytes. METHODS: Using whole cell patch-clamp recording techniques. RESULTS: Est 10μmol·L-1 and 100 μmol· L-1 decreased the action potential duration, APD50, from (474± 71) ms to (330± 75) ms and (229±67) ms (n =7 cells of 7 guinea pigs, P < 0.05), respectively. Est 100 μmol·L-1 also decreased APD90 from (587±60) ms to (418±79) ms (n=7, P<0.05). Est inhibited IK tail current (IK·tail) concentration-dependently. IK·tail was depressed 53 % (n =5, P <0.05) at 10 μmol·L-1 and 80 % (n = 5, P < 0.01) at 100 μmol· L-1 compared with control. Est≥10 μmol·L-1 blocked IKl. The maximal inhibition of inward current of IKl occurred at - 100 mV test potential was 49 % (n = 5, P < 0.01) and outward current of 7K1 at - 40 mV was 72 % (n = 5, P < 0.01). The reverse potential shifted negatively, from -70 to -76mV. CONCLUSION: Est possessed blocking effects on both IKl and IK channels in guinea pig ventricular myocytes.更多还原