Arito H, Uchiyama I, Yokoyama E
National Institute of Industrial Health, Kawasaki, Japan.
Ind Health. 1992;30(1):23-34. doi: 10.2486/indhealth.30.23.
Effects of exposure to O3 on EEG activity, sleep-wakefulness and heart rate were examined using conscious rats which had been chronically implanted with electrodes for EEG, EMG and ECG recordings. Exposure to 0.5 ppm O3 for 6 hrs and 1.0 ppm O3 for 3 hrs suppressed amounts of wakefulness (W) and paradoxical sleep (PS) at the expense of an increase in slow-wave sleep (SWS), and lowered the amplitude of fast EEG waves and heart rate (HR). The lowered EEG amplitude and the suppressed PS recovered more rapidly during the post-exposure period than did the lowered HR. The ip administration of atropine sulfate blocked the suppressed W, the increased SWS and the lowered HR, while the lowered EEG amplitude and the suppressed PS were not blocked. These observations suggest that the O3-induced bradycardia results from enhanced activity of cardiac parasympathetic nerves and that the O3-induced changes in W and SWS result secondarily from some circulatory factor including the bradycardia.
使用长期植入电极用于脑电图（EEG）、肌电图（EMG）和心电图（ECG）记录的清醒大鼠，研究了暴露于臭氧（O3）对EEG活动、睡眠-觉醒和心率的影响。暴露于0.5 ppm O3 6小时和1.0 ppm O3 3小时，以慢波睡眠（SWS）增加为代价，抑制了觉醒量（W）和异相睡眠（PS），并降低了快速EEG波的振幅和心率（HR）。暴露后，降低的EEG振幅和受抑制的PS比降低的HR恢复得更快。腹腔注射硫酸阿托品可阻断受抑制的W、增加的SWS和降低的HR，而降低的EEG振幅和受抑制的PS未被阻断。这些观察结果表明，O3诱导的心动过缓是由心脏副交感神经活动增强引起的，O3诱导的W和SWS变化继发于包括心动过缓在内的一些循环因素。
