牛磺酸镁抗缺氧/复氧致大鼠心肌细胞瞬时外向钾离子通道异常的研究

IM To clarify the antiarrhythmic mechanism of taurine magnesium coordination compound(TMCC), we observed the effect of TMCC on abnormal Transient Outward Potassium Current (Ito) induced by hypoxia/reoxygenation in rat venticular cardiomyocytes . METHODS Enzymatic dissociation was used to get single rat ventricular myocytes and whole-cell patch clamp was used to record Ito in ventricular cardiomyocytes suffered from hypoxia/reoxygenation in rat under amiodarone and TMCC at different concentrations. RESULTS In hypoxia/reoxygenation model,peak Ito increased from (8.40±0.66) pA/pF to (13.50±0.41) pA/pF (n=6,P<0.01). TMCC 200 μmol/L, 400 μmol/L and amiodarone 24.24 μmol/L restored peak Ito. The I-V curve of Ito upward shift induced by hypoxia/reoxygenation were inhibited by TMCC and amiodarone. Compared to control group ,hypoxia/reoxygenation shifted Ito steady-state activation curves to the left which made activation of potassium channel quickly. TMCC 200 μmol/L,400 μmol/L and amiodarone 24.24 μmol/Lrestored the left-shifted activation process.However the steady-state inactivation curves remained unchanged. CONCLUSION TMCC 200 μmoloL-1 and 400 μmol/L concentration-dependently restored the hypoxia/reoxygenation-induced abnormal Ito by inhibiting activate process.