甲状腺素诱导的豚鼠肥厚心肌中快速激活的延迟整流钾电流和内向整流钾电流离子通道特征

在甲状腺素诱导的豚鼠心肌肥厚模型上，采用膜片钳全细胞技术，研究病变心肌细胞APD，Ikr及Ik1离子通道特征，以及药物治疗后其离子通道的改变。结果表明，肥厚心肌细胞APD明显缩短，静息电位及动作电位幅度不变，Ikr及Ik1均显著增加，反转电位不变。经propranolol治疗后，心肌APD，Ikr及Ik1均有明显改善，不影响Ikr的反转电位，但使Ik1反转电位向负的方向偏移。以上结果提示，甲状腺素诱发的心肌肥厚加重心律失常的严重性与增加Ikr及Ik1有关，作用多通道的复合型抗心律失常药有较好的治疗作用。

Rapidly Activating Delayed Rectifier K Current and Inward Rectifier K Current in Cardiocytes from Hypertrophied Guinea Pig Hearts Induced by Thyroxine

We studied the characteristics of action potential duration (APD), Ikr and Ik1 recorded from hypertrophied guinea pig ventricular myocytes induced by thyroxine, by means of the whole-cell patch-clamp techniques. In hypertrophied ventricular myocytes, APD was markedly shortened, and resting potential and action potential amplitude was unaffected; The amplitude of steady-state Ikr and Ik1 were significantly increased, and Erev of both did not changed. After using propranolol therapy, APD, Ikr and Ik1 were ameliorated, Erev of Ikr was not affected, and Erev of Ik1 was made more negative. The results suggest that the enhanced Ikr or Ik1 in hypertrophied ventricular myocytes might be one of the causes for increasing incidence of arrhy thmias, and antiarrhythmic agents by blocking multiple ion channels may produce their better therapeutic action.