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目的:研究盐酸小檗碱(berberine,Ber)对甲状腺素性豚鼠心肌病中延迟整流外向钾电流中快激活成分(Ⅰ_(Kr))和慢激活成分(Ⅰ_(Ks))及内向整流电流(Ⅰ_(K1))的抑制作用.方法:豚鼠腹腔注射L-甲状腺素造成心肌病后,分离单个心肌细胞,用全细胞膜片钳技术记录钾电流.结果:在心肌病细胞的,Ⅰ_(Kr),Ⅰ_(Ks)和Ⅰ_(K1)电流密度均明显增大,Ber 30 mmoL/L分别抑制心肌病细胞Ⅰ_(Kr) 22.8%(+10 mV)和Ⅰ_(Ks) 29.5%(+80 mV),其对Ⅰ_(Ks)的阻断作用大于Ⅰ_(Kr).Ber 30 mmol/L也能阻断心肌病细胞Ⅰ_(K1) 29.1%(+120 mV),但不影响其反转电位.Ber(1～300 mmol/L)浓度依赖性地阻断心肌病细胞Ⅰ_(Kr)及Ⅰ_(Ks),其IC_(50)分别为76mmol/L和55.37 mmol/L.结论:甲状腺素性心肌病中出现异常增大的Ⅰ_(Ks),Ⅰ_(Kr)及Ⅰ_(K1)离子流,Ber有明显阻断作用.“,”Aim: To study the effects of berberine( Ber) on the rapidly activating component( Ⅰ_(Kr)), the slowly activating component(Ⅰ_(Ks)) of the delayed rectifier potassium current and the inward rectifier potassium current(Ⅰ_(K1)) in cardiomyopathic guinea pig ventricular myocytes. Methods: After guinea pigs were ip L-thyroxine 0. 5 mg/kg for 10 d, their hearts were cardiomyopathic. Then whole cell patch-clamp recording technique was used to observe the effect of 30 μmol/L Ber on the Ⅰ_(Kr), Ⅰ_(Ks) and Ⅰ_(K1) in cardiomyopathic guinea pig ventricular myocytes. Results: In cardiomyopathic guinea pig ventricular myocytes, Ber 30 μmol/L markedly inhibited Ⅰ_(Kr) and Ⅰ_(Ks) by 22. 8% and 29. 5% at + 10 mV and + 80 mV, respectively. The effect of Ber on Ⅰ_(Ks) was greater than that on Ⅰ_(Kr). Ber 30 μmol/L also inhibited the inward component of Ⅰ_(K1) by 29. 1% at + 120 mV, but the reverse potential of Ⅰ_(K1) was unaffected. Ber( 1-300 μmol/L) was shown to inhibit Ⅰ_(Kr) and Ⅰ_(Ks) in a concentration-dependent manner. Their IC_(50), were 76. 74 μmol/L and 55. 37 μmol/L, respectively. Conclusion: Ber inhibited Ⅰ_(Kr),Ⅰ_(Ks) and Ⅰ_(K1) in cardiomyopathic guinea pig ventricular myocytes, which may be important in understanding the antiarrhythmic effects of this drug.