Effects of Sleep Deprivation on Action Potential and Transient Outward Potassium Current in Ventricular Myocytes in Rats

BACKGROUND: Sleep deprivation contributes to the development and recurrence of ventricular arrhythmias. However, the electrophysiological changes in ventricular myocytes in sleep deprivation are still unknown. MATERIAL/METHODS: Sleep deprivation was induced by modified multiple platform technique. Fifty rats were assigned to control and sleep deprivation 1, 3, 5, and 7 days groups, and single ventricular myocytes were enzymatically dissociated from rat hearts. Action potential duration (APD) and transient outward current (I(to)) were recorded using whole-cell patch clamp technique. RESULTS: Compared with the control group, the phases of APD of ventricular myocytes in 3, 5, and 7 days groups were prolonged and APD at 20% and 50% level of repolarization (APD(20) and APD(50)) was significantly elongated (The APD(20) values of control, 1, 3, 5, and 7 days groups: 5.66±0.16 ms, 5.77±0.20 ms, 8.28±0.30 ms, 11.56±0.32 ms, 13.24±0.56 ms. The APD(50) values: 50.66±2.16 ms, 52.77±3.20 ms, 65.28±5.30 ms, 83.56±7.32 ms, 89.24±5.56 ms. P<0.01, n=18). The current densities of I(to) significantly decreased. The current density-voltage (I–V) curve of I(to) was vitally suppressed downward. The steady-state inactivation curve and steady-state activation curve of I(to) were shifted to left and right, respectively, in sleep deprivation rats. The inactivation recovery time of I(to) was markedly retarded and the time of closed-state inactivation was markedly accelerated in 3, 5, and 7 days groups. CONCLUSIONS: APD of ventricular myocytes in sleep deprivation rats was significantly prolonged, which could be attributed to decreased activation and accelerated inactivation of I(to).