| [Objective]To observe the effects of Oxymatrine on sodium current, L-type calcium current,inward rectifier potassium current in isolated ventricular myocytes of guinea pigs and transient outward potassium current in isolated ventricular myocytes of rats; to explore the mechanisms underlying the antiarrhythmic effect of Oxymatrine at the ionic channel level. This can provide a kind of methodology for researching, exploiting effective component of Chinese herbal medicine.[Methods]Single ventricular myocyte of guinea pigs and rats were isolated by enzymaticdissociation. The whole-cell patch clamp recording technique was used to record the change of currents of INa, IK1, Ito and Ica-L influenced by Oxymatrine.[Results]1. Oxymatrine decreased the sodium channel current in a dose-dependent andvoltage-dependent manner. IC50 was 86.5 mol/L. (1) Oxy at 100 mol.L-1 decreased current density by 45%(P<0.01). Peak current density were (-13.41+6.95 vs -8.53 3.70pA/pF, n=9, P<0.01). The current-voltage curve was shifted upwardwhile active potential(-60mV), peak potential(-30mV) and reverse potential(+25mV) had no changes. (2)The activation curve was not altered. V50 were (-44.84+6.76 vs -52.63+ 1.39mV, n=9, P>0.05)and Slope were (2.12 + 0.37 vs 2.2 + 0.31, n=9, P>0.05). (3)The inactivation curve was shifted toward more negative potential. Vso were (-71.40 + 2.82 vs -74.99+1.10mV, n=9, P<0.01). Slope were (-6.83+2.82 vs -3.67+ 1.50, n=9, P<0.01). (4)The recovery curve had significant changes. Vso were (7.51+0.87 vs 13.59 4.27mV, n=6, P<0.05). Slope were (2.38 0.64 vs 5.67 + 2.84, n=6, PXJ.05).2. Oxy Immol/L had no effect on inward rectifier potassium channel current. On -110mV membrane potential, current density were (-21.87 + 5.56 vs -18.37 + 6.77pA/pF, n=6, P>0.05).3. Oxy Immol/L had no effect on transient outward potassium channel current. On +50mV membrane potential, current density were (12.28 + 5.50 vs 11.47 + 2.92pA/pF, n=6, PXJ.05). The activation curve indicated that V50 were (28.67 + 6.57 vs 26.92 5.78mV, n=6, PXJ.05) and Slope were (16.75 3.75 vs 18.93 + 3.02, n=6, P>0.05). The inactivation curve indicated that V50 were (-35.70 + 3.91 vs -29.34+ 1.64mV, n=6, P>0.05) and Slope were (-3.50 + 0.49 vs -3.65 + 0.29, n=6, P>0.05). The recovery curve showed no significant changes. Vso of recovery were (23.01 + 3.36 vs 24.5 5.1mV, n=6, P>0.05). S of recovery were (12.93 + 2.45 vs 9.41 +2.03, n=6, P>0.05).4. Oxy increased the L-type calcium channel current in a dose-dependent and voltage-dependent manner. ECso was 0.3 mol/L. Oxy at 0.1 mol.L-1 increased current density by 30%(P<0.01). Peak current density were (-6.57+2.98 vs -8.36+ 3.48pA/pF, n=8, P<0.01). The current-voltage curve was shifted downward while active potential(-40mV), peak potential(OmV) and reverse potential(+50mV) had no changes. (l)The activation curve was shifted to more negative potential. Vso of activation were (-10.61 +3.57 vs -14.39+6.75mV, n=8, P<0.05). S of activationwere (4.24+1.30 vs 3.92 + 1.154, n=8, P>0.05). (2)The inactivation curve had no significant change, showing that V50 were (-17.54+0.11 vs -17.60+1.30mV, n=5, P>0.05) and Slope were (-6.56 0.12 vs -6.63 0.21, n=5, P>0.05). (3)The recovery curve indicated that V50 were (50.15 10.79 vs 63.31 7.24mV, n=5, P>0.05) and S were (30.32 7.99 vs 26.89+1.61, n=5, P>0.05). The recovery curve was not altered.[ Conclusion ]Oxymatrine blocks INa at its inactive state by a dose-dependent andvoltage-dependent manner. Oxymatrine has no significant effect on Ito and IK1 . Oxymatrine increases the L-type calcium channel current in a dose-dependent and voltage-dependent manner, and probably effects on its active state.
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