Huupponen E, Maksimow A, Lapinlampi P, Särkelä M, Saastamoinen A, Snapir A, Scheinin H, Scheinin M, Meriläinen P, Himanen S-L, Jääskeläinen S
Department of Clinical Neurophysiology, Tampere University Hospital, Finland.
Acta Anaesthesiol Scand. 2008 Feb;52(2):289-94. doi: 10.1111/j.1399-6576.2007.01537.x. Epub 2007 Nov 14.
Dexmedetomidine, a selective alpha(2)-adrenoceptor agonist, induces a unique, sleep-like state of sedation. The objective of the present work was to study human electroencephalogram (EEG) sleep spindles during dexmedetomidine sedation and compare them with spindles during normal physiological sleep, to test the hypothesis that dexmedetomidine exerts its effects via normal sleep-promoting pathways.
EEG was continuously recorded from a bipolar frontopolar-laterofrontal derivation with Entropy Module (GE Healthcare) during light and deep dexmedetomidine sedation (target-controlled infusions set at 0.5 and 3.2 ng/ml) in 11 healthy subjects, and during physiological sleep in 10 healthy control subjects. Sleep spindles were visually scored and quantitatively analyzed for density, duration, amplitude (band-pass filtering) and frequency content (matching pursuit approach), and compared between the two groups.
In visual analysis, EEG activity during dexmedetomidine sedation was similar to physiological stage 2 (S2) sleep with slight to moderate amount of slow-wave activity and abundant sleep spindle activity. In quantitative EEG analyses, sleep spindles were similar during dexmedetomidine sedation and normal sleep. No statistically significant differences were found in spindle density, amplitude or frequency content, but the spindles during dexmedetomidine sedation had longer duration (mean 1.11 s, SD 0.14 s) than spindles in normal sleep (mean 0.88 s, SD 0.14 s; P=0.0014).
Analysis of sleep spindles shows that dexmedetomidine produces a state closely resembling physiological S2 sleep in humans, which gives further support to earlier experimental evidence for activation of normal non-rapid eye movement sleep-promoting pathways by this sedative agent.
右美托咪定是一种选择性α₂肾上腺素能受体激动剂，可诱导出一种独特的、类似睡眠的镇静状态。本研究的目的是研究右美托咪定镇静期间的人类脑电图（EEG）睡眠纺锤波，并将其与正常生理睡眠期间的纺锤波进行比较，以检验右美托咪定通过正常促睡眠途径发挥作用的假说。
在11名健康受试者接受浅度和深度右美托咪定镇静（靶控输注设定为0.5和3.2 ng/ml）期间，以及10名健康对照受试者的生理睡眠期间，使用熵模块（GE医疗）从双极额极-额外侧导联连续记录脑电图。对睡眠纺锤波进行视觉评分，并对其密度、持续时间、振幅（带通滤波）和频率成分（匹配追踪法）进行定量分析，然后在两组之间进行比较。
在视觉分析中，右美托咪定镇静期间的脑电图活动类似于生理睡眠第2阶段（S2），有少量至中等量的慢波活动和丰富的睡眠纺锤波活动。在定量脑电图分析中，右美托咪定镇静期间和正常睡眠期间的睡眠纺锤波相似。在纺锤波密度、振幅或频率成分方面未发现统计学上的显著差异，但右美托咪定镇静期间的纺锤波持续时间（平均1.11秒，标准差0.14秒）比正常睡眠期间的纺锤波（平均0.88秒，标准差0.14秒；P = 0.0014）更长。
对睡眠纺锤波的分析表明，右美托咪定在人类中产生的状态与生理S2睡眠非常相似，这进一步支持了早期的实验证据，即这种镇静剂可激活正常的非快速眼动促睡眠途径。
