牛磺酸镁配合物对缺氧复氧致大鼠心肌细胞瞬时外向钾离子通道异常的影响

目的研究牛磺酸镁配合物(TMCC)对缺氧复氧损伤所致大鼠心肌细胞异常瞬时外向钾电流(Ito)的影响。方法采用Langendoff逆行主动脉灌注酶消化法急性分离大鼠单个心室肌细胞,分为空白对照组、模型组、100μmol.L-1 TMCC组、200μmol.L-1 TMCC组、400μmol.L-1 TMCC组和24.24μmol.L-1胺碘酮组,均n=6。缺氧钾外液模拟缺氧15 min后用有氧钾外液复氧5 min制缺氧复氧模型。应用全细胞膜片钳技术记录Ito。结果与空白对照组相比,模型组大鼠心室肌细胞Ito峰值显著增大(13.50±0.41 pA.pF-1 vs.8.40±0.66 pA.pF-1,P<0.01),I-V曲线上移,Ito激活曲线左移;200、400μmol.L-1 TMCC组和胺碘酮组均可使因缺氧复氧损伤增大的Ito减小(均P<0.01),使I-V曲线下移并纠正左移的激活曲线。各组对稳态失活曲线均无显著影响,曲线无移动(均P>0.05)。结论 TMCC可通过抑制钾通道的激活过程对抗缺氧复氧引起的Ito增大,提示该作用可能是TMCC抗缺氧复氧诱发心律失常的作用机制之一。

Effect of taurine-magnesium coordination compound on abnormal transient outward potassium current induced by hypoxia-reoxygenation in cardio-myocytes of rats

AIM To observe the effect of taurine-magnesium coordination compound(TMCC)on abnormal transient outward potassium current(Ito)induced by hypoxia-reoxygenation in cardiomyocytes of rats.METHODS Enzymatic dissociation was used to get single rat ventricular myocyte through Langendoff retrograde aortic perfusion.Myocytes were divided into control group,model group,100 μmol·L-1 TMCC group,200 μmol·L-1 TMCC group,400 μmol·L-1 TMCC group and 24.24 μmol·L-1 amiodarone group(n = 6).Hypoxia-reoxygenation model was prepared by hypoxic potassium extracellular fluid for 15 min and normal potassium extracellular fluid for 5 min.The whole-cell patch clamp was used to record Ito.RESULTS Compared with the control group,the peak of Ito in the hypoxia-reoxygenation model increased significantly(13.50 ± 0.41 pA·pF-1 vs.8.40 ± 0.66 pA·pF-1,P < 0.01),the I-V curve of Ito shifted upward,and the steady-state activation curve shifted toward negative potential.The 200,400 μmol·L-1 TMCC groups and the amiodarone group restored the peak of Ito(P < 0.01),shifted the I-V curve downward,and restored the left-shifted activation process.The steady-state inactivation curves remained unchanged in all groups(P > 0.05).CONCLUSION TMCC restored the hypoxia-reoxygenation-induced abnormal Ito through inhibiting activation process,which suggested that the effect may be one of the mechanisms of anti-hypoxia-reoxygenation induced arrhythmias of TMCC.