RESUMO
OBJECTIVE To explore the mechanism of methylamphetamine (MA) on heart toxicity. METHODS The effects of MA on delayed rectifier potassium current (IK) and action potential (AP) were analyzed in isolated decreased AP from 121.6 to 106.0 mV and delayed the action potential duration (APD), but had no effect on the resting potential. The 10%, 25%, 50%, 75% and 90% of APD (APD10, APD25, APD50, APD75 and APD90)inhibited the membrane potential of rapidly activating delayed rectifier potassium current (IKr) and slowly activating delayed rectifier potassium current (IKs), downward shifted the Ⅰ -Ⅴ curve, but had no effect on the curve shape and could be partly recovered after flushing. The tail current IKr was blocked concentration-dependently after simiarly inhibited by MA. CONCLUSION MA has inhibitory effects on Ik and AP in ventricular myocytes,which may be one of the possible electrophysiological mechanisms of the cardiac damage caused by MA.