Objective To investigate the alterations of cardiac electrophysiological properties and substantial mechanism and find the stable arrhythmia mouse model in Kunming (KM) and C57BL6/J (C57) mice.Methods Electrocardiogram recordings were used to analyze the QT interval in vivo

and mono- phasic action potential of right and left ventricular epicardium was recorded to elicit changes of action potential duration (APD) in conventional and programmed electrical stimulation (PES). Transient outward potassium current (Ito) was recorded via whole-cell patch-clamp technique in single right and left epicardial myocytes.Results QT interval was prolonged in KM mice relative to C57 mice (62.51?4.47 ms vs. 52.59?4.85 ms

P<0.05). The APD at 50% repolarization of the left ventricular epicardium (18.60?0.91 ms vs. 12.90?0.35 ms)

and APDs at 50% (17.31?6.05 ms vs. 12.00?3.24 ms) and 70% repolarization (36.13?5.32 ms vs. 21.95?8.06 ms) of the right ventricular epicardium in KM mice were significantly prolonged compared with C57 mice

respectively (all P<0.05). KM mice were more sensitive to PES-induced ventricular tachycardia (25%

3 of 12 hearts)

and especially to Burst-induced ventricular tachycardia (50%

6 of 12 hearts) compared with C57 mice

which were 20% (2 of 10 hearts) and 30% (3 of 10 hearts) respectively. Ito densities both in the left and right ventricular epicardial myocytes from KM mice were significantly decreased compared with C57 mice

respectively (all P<0.01). Conclusion Our data showed that KM mice with the prolonged QT interval and APD are vulnerabilities to ventricular arrhythmia

which are attributed to lower Ito densities in ventricular myocytes obtained from KM mice than that from C57 mice.