Aim To investigate the antiarrhythmic mechanism of taurine magnesium coordination compound on abnormal inward rectifier potassium current ( Ik1 ) induced by hypoxia-reoxygenation in cardiomyocytes of rats. Methods Enzymatic dissociation through Langendorff retrograde aortic perfusion was used to get single rat ventricular myocytes. In voltage clamp mode, whole-cell patch clamp was used to record Ik1 in normal cardiomyocytes and single rat ventricular cardiomyocytes of arrhythmia induced by hypoxia-reoxygenation. Results TMCC had no effect on Ik1 from normal cardiomyocytes. Compared to the control group,the inward current peak of Ik1 in the hypoxia-reoxygenation model was reduced significantly ( -13. 05 ± 1. 431 pA · pF-1 vs -6. 94 ±0. 59 PA · pF-1, n = 6 P < 0. 01 ), and the inward current I-U curve of Ik1 shifted upward. Compared with hypoxia / reoxygenation group, TMCC( 100,200,400 μmol · L-1 )restored the inward current peak of Ik1 to ( -7. 21 ± 0. 79 ) pA · pF-1,( - 7. 28 ± 0. 22 ) pA · pF-1, ( -10.96 ± 0. 78) PA · PF-1(n = 6, P < 0. 01 ), 24. 24μmol · L-1 amiodarone restored it to ( - 8. 80± 0. 97 ) pA · pF-1 ,and shifted the I-V curve downward. Besides,compared to the control group,the outward current peak of Ik1 in the hypoxia-reoxygenation model was reduced significantly( 2. 43 ± 0. 32 pA · pF-1 vs 1.31 ± 0.28 pA · pF-1,P<0. 01 ),and the outward current I-V curve of Ik1 shifted downward. Compared with hypoxia / reoxygenation group, TMCC ( 100,200,400 μmol · L-1 )restored the outward current peak to ( 0. 90 ± 0. 14 ) pA · pF-1, ( 1. 84 ± 0. 46 ) pA · pF-1,( 2. 36 ± 0. 40 ) pA · pF-1,24. 24 μmol · L-1 amiodarone restored it to ( 2. 16 ± 0. 69 )pA · pF-1, and shifted the I-V curve upward. Conclusions TMCC has no effect on Ik1 in normal cardio-myocytes. However, TMCC can restore the inward current and the outward current of Ik1, which is reduced by hypoxia-reoxygenation, which suggests that the effect may be one of the mechanisms of anti-hypoxia-reoxy-genation-induced arrhythmias of TMCC.%目的 观察牛磺酸镁配合物(taurine magnesium coordination compound,TMCC)对缺氧/复氧损伤所致大鼠心肌细胞异常内向整流钾通道电流(Ik1)的影响.方法 采用Langendorff逆行主动脉灌流酶溶液消化法急性分离大鼠单个心肌细胞,在电压钳模式下,应用全细胞膜片钳技术记录不同浓度TMCC对正常细胞和不同浓度TMCC及胺碘酮对缺氧/复氧模型细胞内向整流钾通道电流Ik1的变化.结果 不同浓度TMCC对正常大鼠心肌细胞的Ik1无明显性影响.缺氧/复氧能使Ik1内向电流峰值从(-13.05±1.43)pA·pF-1降至(-6.94±0.59)pA·pF-1(n=6,P<0.01),内向电流曲线上移.与缺氧/复氧组相比,TMCC(100、200、400 μmol·L-1)可使减小的内向电流峰值分别恢复为(-7.21±0.79)pA·pF-1、(-7.28±0.22)pA·pF-1、(-10.96±0.78)pA·pF-1(n=6,P<0.01),24.24μmol·L-1胺碘酮使其恢复为(-8.80±0.97)pA·pF-1.TMCC(100、200、400 μmol·L-1)和胺碘酮均可使上移的内向电流曲线下移.缺氧/复氧使大鼠心肌细胞Ik1外向电流峰值从(2.43±0.32)pA·pF-1降至(1.31±0.28)pA·pF-1,I-V曲线下移.与缺氧/复氧组相比,TMCC(100、200、400μmol·L-1)可使减小的外向电流分别恢复为(0.90±0.14)pA·pF-1、(1.84±0.46)pA·pF-1、(2.36±0.40)pA·pF-1、24.24μmol·L-1 胺碘酮使其恢复为(2.16±0.69)pA·pF-1.TMCC(100、200、400 μmol·L-1)和胺碘酮均可使下移的外向电流曲线上移.结论 TMCC对正常心肌细胞Ik1无影响,但能恢复缺氧/复氧减小的Ik1内向电流和外向电流峰值.提示TMCC对Ik1的作用可能是其发挥抗心律失常的机制之一.
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