中文摘要：

目的：以正常心肌为对照,研究甲状腺素心肌病左右心室瞬时外向钾电流（Ito）不均一性变化。方法：SD大鼠以0.5mg/kgipL-甲状腺素10d后造成心肌病,以急性酶解法消化大鼠心脏,得到左右心室单个心肌细胞,用全细胞膜片钳技术分别记录Ito。结果：正常心肌细胞中左右心室的Ito存在一定差异,但不明显,然而在甲状腺素心肌病模型中这种差异显著增大。去极化电压为＋40mV时,Ito右心室的电流密度从（9.23±0.84）pA/pF增强至（11.19±1.73）pA/pF,而左心室的电流密度从（6.99±1.14）pA/pF降至（4.95±1.84）pA/pF,且离散度增大。病变的右心室细胞半失活电压V1/2从（-68.85±1.37）mV右移至（-49.86±0.69）mV;正常心肌细胞的左右心室失活后恢复常数τ相当,而在病变心肌左右心室的τ值离散度显著增大,分别为（79.16±7.04）ms和（53.19±3.72）ms。结论：在心脏病变中左右心室Ito的不均一性增大可能是肥厚心脏导致心律失常的重要离子基础之一。

英文摘要：

AIM：To study the electrical heterogeneity of transient outward potassium current （Ito） in left and right ventricular myocytes of cardiomyopathy rat. METHODS： The rats were peritoneally injected with L-thyroxine 0.5 mg/kg for 10 d to establish the model of ventricular hypertrophy. The right and left ventricular parts of the heart were separated and the ventricular myocytes were prepared by step digestion using enzyme solution. Ito was recorded by using whole cell patch clamp technique. The change of the electrical heterogeneity was determined. RESULTS： The electrical heterogeneity of Ito existed in the normal myocytes of left and right ventricles. In the myocytes of left and right ventricles isolated from the cardiomyopathy rats,the electrical heterogeneity was enhanced obviously and showed statistical difference. At ＋40 mV depolarizing test potential,the current density of Ito in the myocytes of right ventricle was increased from （9.23±0.84） pA/pF to （11.19±1.73） pA/pF,while the current density of Ito in the myocytes of left ventricle was decreased from （6.99±1.14） pA/pF to （4.95 ±1.84） pA/pF and the dispersion was increased. The V1/2 of right ventricle steady inactivation was increased significantly [from （-68.85±1.37） mV to （-49.86±0.69） mV]. The time constant τ of de-inactivation changed significantly [τ left=（79.16±7.04） ms,τ right=（53.19±3.72） ms]. CONCLUSION： Enhanced electrical heterogeneity of Ito in the left and right ventricular myocytes of cardiomyopathy rat may represent one of the important ionic mechanisms for some arrhythmia caused by myocardial hypertrophy.