Effects of taurine-magnesium coordination compound on abnormal sodium channel induced by hypoxia-reoxygenation in rat ventricular myocytes
10.3969/j.issn.1001-1978.2014.10.012
- VernacularTitle:牛磺酸镁对缺氧/复氧致大鼠心室肌细胞钠离子通道异常的影响
- Author:
Tianshen CONG
;
Minghui ZHANG
;
Haiyan HE
;
Yongqiang YIN
;
Hong WU
;
Yi KANG
;
Jianshi LOU
- Publication Type:Journal Article
- Keywords:
taurine-magnesium coordination com-pound (TMCC);
arrhythmia;
ventricular myocytes;
sodium channel;
whole-cell patch technique;
amioda-rone
- From:
Chinese Pharmacological Bulletin
2014;(10):1382-1387
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the antiarrhythmic mechanism of taurine-magnesium coordination com-pound on abnormal sodium current channel ( INa ) in-duced by hypoxia-reoxygenation in ventricular myocytes of rats. Methods Single ventricular myocytes were i-solated from each rat heart using enzymatic dissociation through Langendorff retrograde aortic perfusion. Whole-cell patch clamp was applied in voltage clamp mode to record INa both in normal ventricular myocytes and single ventricular myocytes of arrhythmia induced by hypoxia-reoxygenation. Results The peak density of INa was changed from ( 56. 89 ± 2. 07 ) pA/pF to (35. 05 ± 1. 52) pA/pF( n=6, P <0. 01 vs control) by hypoxia-reoxygenation with the INa I-V curve shifting upward. TMCC(200, 400 μmol·L-1)was able to re-store the reduction caused by H/R to (35. 78 ± 1. 95) pA/pF, (41. 52 ± 0. 86) pA/pF, (n=6,P <0. 01) and (48. 34 ± 0. 99) pA/pF(n=6,P<0. 01) respec-tively, but not at 100 μmol·L-1(n=6, P>0. 05), in a concentration-dependent manner, while amioda-rone restored it to (39. 44 ± 1. 24) pA/pF (n=6,P<0. 01 ) . Both high concentration of TMCC and amioda-rone could shift the I-V curve downward. In addition, TMCC and amiodarone could restore the INa inactivation curve and slow down its inactivation, whereas the acti-vation curves showed no significant differences among groups. Conclusion TMCC(200,400 μmol·L-1) could restore the H/R induced INa reduction and shift the I-V curve downward by inhibiting steady-state inac-tivation, which is suggested to be one of the mecha-nisms of the antiarrhythmic effects of TMCC in hypoxia-reoxygenation model.
