title: Effects of sleep deprivation on action potential and transient outward potassium current in ventricular myocytes in rats.
abstract: 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.
  
  
  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 (Ito) 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 (APD20 and APD50) was significantly elongated (The APD20 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 APD50 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 Ito significantly decreased. The current density-voltage (I-V) curve of Ito was vitally suppressed downward. The steady-state inactivation curve and steady-state activation curve of Ito were shifted to left and right, respectively, in sleep deprivation rats. The inactivation recovery time of Ito 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 Ito.
authors.affiliation: Institute of Geriatric Cardiology, The General Hospital Of People's Liberation Army, Beijing, China (mainland).
authors.forename: Zhou
authors.initials: Z
authors.lastname: Fang
authors.affiliation: Institute of Geriatric Cardiology, The General Hospital Of People's Liberation Army, Beijing, China (mainland).
authors.forename: Yi-Peng
authors.initials: YP
authors.lastname: Ren
authors.affiliation: Institute of Geriatric Cardiology, The General Hospital Of People's Liberation Army, Beijing, China (mainland).
authors.forename: Cai-Yi
authors.initials: CY
authors.lastname: Lu
authors.affiliation: Institute of Geriatric Cardiology, The General Hospital Of People's Liberation Army, Beijing, China (mainland).
authors.forename: Yang
authors.initials: Y
authors.lastname: Li
authors.affiliation: Institute of Geriatric Cardiology, The General Hospital Of People's Liberation Army, Beijing, China (mainland).
authors.forename: Qiang
authors.initials: Q
authors.lastname: Xu
authors.affiliation: Institute of Geriatric Cardiology, The General Hospital Of People's Liberation Army, Beijing, China (mainland).
authors.forename: Li
authors.initials: L
authors.lastname: Peng
authors.affiliation: Institute of Geriatric Cardiology, The General Hospital Of People's Liberation Army, Beijing, China (mainland).
authors.forename: Yong-Yan
authors.initials: YY
authors.lastname: Fan
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D006352:Heart Ventricles / Q000473:pathology*; D015640:Ion Channel Gating; D008297:Male; D032383:Myocytes, Cardiac / Q000378:metabolism*; D015221:Potassium Channels; D017207:Rats, Sprague-Dawley; D012892:Sleep Deprivation / Q000503:physiopathology*; D013997:Time Factors
chemical_list: D015221:Potassium Channels