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.

Objective To investigate the effects of single i.v. subanesthetic dose of ketamine on heart rate, blood pressure and oxygen saturation for antidepressant treatment. Methods Patients with severe depressive disorder were randomized to ketamine group (n=13) and control group (n=14). Ketamine group received ketamine (0.5mg/kg) single injection whereas control group received saline single injection. Escitalopram (10 mg/d) were orally administered for 4 weeks simultaneously. Comparisons were made on the heart rate, blood pressure and oxygen saturation at baseline, 40 min, 100 min, and 280 min after injection between the two groups. Results The main effects of time but not group were significant for all parameters including heart rate, systolic blood pressure and diastolic blood pressure, (P＜0.05). Interaction of time×group was significant (P＜0.05). All parameters including heart rate (F=16.85, P＜0.01), systolic blood pressure (F=15.82, P＜0.01) and diastolic blood pressure (F=8.63, P＜0.01) with time were significant in ketamine group. The heart rate, systolic blood pressure and diastolic blood pressure in ketamine group were significantly higher at 40 min than at other time points (P＜0.05), while were no significant difference among other time points (P＞0.05). There was no statistical significance of main effect of time, group and interaction of time×group in oxygen saturation between the two groups (P＞0.05). Conclusion Single subanesthetic dose ketamine intravenous drip for antidepressant therapy may cause a transient increase in heart rate and blood pressure.