OBJECTIVETo 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.

METHODSElectrocardiogram 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.

RESULTSQT 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 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).

CONCLUSIONOur 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.