Correspondence  |   August 2017
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Author Notes
  • Peking University First Hospital, Beijing, China (D.-X.W.). wangdongxin@hotmail.com
  • (Accepted for publication May 8, 2017.)
    (Accepted for publication May 8, 2017.)×
Article Information
Correspondence
Correspondence   |   August 2017
In Reply
Anesthesiology 8 2017, Vol.127, 398-399. doi:10.1097/ALN.0000000000001723
Anesthesiology 8 2017, Vol.127, 398-399. doi:10.1097/ALN.0000000000001723
We agree with Dr. Goucher et al. that low-dose dexmedetomidine infusion did not restore the normal sleep architecture because stage 3 non–rapid eye movement sleep and rapid eye movement (REM) sleep remained significantly decreased or absent in our patients.1  This is also the case when dexmedetomidine was administered for sedation in mechanically ventilated patients.2,3  It should be noted that the target subjects were patients in the intensive care unit (ICU) after major surgery in our study1  or receiving mechanical ventilation in another previous study.3  It is well known that significant sleep disturbances such as fragmented sleep, decreased sleep efficiency, increased stage 1 non-REM sleep, and decreased or absent stage 3 non-REM and REM sleep are often present in those patients. Dexmedetomidine partially improved “sleep architecture” through increasing the percentage of stage 2 non-REM sleep (and decreasing the percentage of stage 1 non-REM sleep), a unique property that has also been demonstrated in other clinical studies previously.4 
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