Objective:To investigate the changes of action potential duration(APD) and transmural dispersion of repolarization(TDR) in Canine model of long-QT syndrome type 3(LQT3) in vivo during bradycardia, to explore the the impact of the sodium channel block-mexiletine on this changes, and to provide experimental evidence for the prevention and treatment of ventricular arrhythemia in congenital LQT3. Methord: The monophasic action potentials(MAP) of endocardium, mid-myocardium and epicardium at the anterior ventricular wall were recorded synchronously in vivo by a self-made electrode, sea anemone toxin (ATX-Ⅱ ) was administered intravenously to mimic LQT3 model, the heart rate was controlled by altering atrium pacing cycle length(PCL) after the sinoatrial node been ablated by 40% formaldehyde. Result:The LQT3 model had been made successfully by the intravenous injection of ATX-Ⅱ (3 μg/kg). The TDR had been increased remarkably by the ATX-Ⅱ when the PCL was both 500 ms and 1000 ms (20±4 ms vs 41 ± 9 ms and 39±5 ms vs 83 ±10 ms respectively, P <0. 05), but the net increase of TDR(ⅡTDR) was more remarkable when the PCL was 1000 ms compared to 500 ms (44±13 ms vs 20± 12 ms, P <0. 05) , with the occurrence of early after depolarization(EAD) originated from mid-myocardium and spontaneity ventricular tachycardia. This electrophysiological effect of ATX-Ⅱ could be reversed by mexiletine(20 μg/kg). Conclusion:The occurrence of ventricular tachycardia in LQT3 model is bradycardia dependent, Mexiletine is probably an effective medicine in the prevention and treatment of the sudden cardiac death of congenital LQT3.