Effect Of Taurine-magnesium Coordination Compound On Abnormal Potassium Current In Cardiomyocytes Of Rat

Aim:Taurine magnesium coordination compound(TMCC) was a new effective compound synthesized by our laboratory and had antiarrhymic effects. But the mechanisms of its antiarrhythmic action remaind to be clarified. The aim of this study was to investigate the effects of TMCC on abnormal potassium current in rat ventricular cardiomyocytes suffered from hypoxia/reoxygenation, ouabain or aconitine and to find out the mechanism of antiarrhythmic effect.Methods:Enzymatic dissociation was used to get single rat ventricular myocytes and whole-cell patch clamp was used to record Ito/Ikl in rat ventricular cardiomyocytes suffered from hypoxia/reoxygenation,ouabain,acontine in respectively under amiodarone and different concentration of TMCC.Results:1In hypoxia/reoxygenation model, peak of Ito increased from (8.40±0.66) pA/pF to (13.50±0.41) pA/pF (n=6, P<0.01), which was restored to (12.69±0.99) pA/pF (n=6, P>0.05),(10.60±0.84)pA/pF (n=6, P<0.01),(7.80±0.15) pA/pF (n=6, P<0.01) by TMCC (100,200,400μmol·L-1).24.24μmol·L-1amiodarone restored peak Ito to (7.93±0.43) pA/pF (n=6, P<0.01).The Ito Ⅰ-Ⅴ curves was shifted upward induced by hypoxia/reoxygenation and inhibited by TMCC and amiodarone. Compared to control group, hypoxia/reoxygenation group shifted Ito steady-state activation cures to left, which made activate quickly, TMCC (200,400μmol·L-1) and24.24μmol·L-1amiodarone restored the left shift activation curves, but they had no effects on the inactivation curves.2In arrhythmic model of ventricular cardiomyocytes of rat induced by1μmol·L-1aconitine, peak of Ikl inside current (-100mV) decreased from (-15.44±1.13) pA/pF to (-9.84±1.52) pA/pF, which was restored to (-9.75±1.00) pA/pF (n=5, P>0.05),(-9.84±2.25) pA/pF (n=5, P>0.05),(-14.72±0.70) pA/pF (n=5, P<0.01) by TMCC (100,200,400μmol·L-1).The Ikl inside current Ⅰ-Ⅴ curves were shifted upward induced by aconitine and inhibited by TMCC (400 μmol·L-1) and24.24μmol·L-1amiodarone. aconitine, TMCC,amiodarone had no effects on Ikl outside current.3In arrhythmic model of ventricular cardiomyocytes of rat induced by5μmol·L-1ouabain, peak of Ikl inside current (-100mV) decreased from (-15.44±1.13) pA/pF to (-7.41±0.38) pA/pF, which was restored to (-8.97±0.71) pA/pF (n=5,P<0.05),(-8.88±0.45) pA/pF (n=5,7P<0.05),(-9.20±0.73) pA/pF (n=5,P<0.01) by TMCC (100,200,400μmol·L-1).The Ikl inside current Ⅰ-Ⅴ curves was shifted upward induced by ouabain and inhibited by TMCC (100,200,400μmol·L-1) and24.24μmol·L-1amiodarone. In arrhythmic model of ventricular cardiomyocytes of rat induced by5μmol·L-1ouabain, peak of Ikl outside current (-40mV) decreased from (1.15±0.38) pA/pF to (0.49±0.14) pA/pF, which was restored to (0.49±0.12) pA/pF (n=5, P>0.05),(0.56±0.14) pA/pF (n=5, P>0.05),(0.91±0.40) pA/pF (n=5,P<0.05) by TMCC (100,200,400μmol·L-1). The Ikl outside current Ⅰ-Ⅴ curves was shifted downward induced by ouabain and inhibited by TMCC (400μmol·L-1), and24.24μmol·L-1amiodarone had no effect on the downward shift curves.Conclusions:1TMCC concentration-dependently restored the increased peak of Ito and up-shift of Ⅰ-Ⅴ curves due to hypoxia/reoxygenation by inhibiting activation process, and had no effects on the inactivation process.2TMCC restored the decreased peak of Ikl inside current and up-shift of Ⅰ-Ⅴ curves due to1μmol·L-1aconitine.3TMCC restored the decreased peak of Ikl inside and outside current due to5μmol·L-1ouabain, and restored the up-shift curves of inside currents and the down-shift curves of outside currents.