Search

This study was designed to examine the effects of brief naps taken after lunch on alertness, performance, and autonomic balance. Three groups each comprising ten healthy subjects, who had slept normally at home the previous night, were randomly assigned to groups taking one of three 'lengths of nap (0, 15, and 45 min) after lunch. The P300, an event-related potential which is a neurophysiological correlate of cognitive function, subjective sleepiness (visual analogue scale), and electrocardiogram were measured before, 30 min after, and 3 h after the naps. Each measurement was followed by an English transcription task lasting 90 min. The P300 latency was significantly shorter after the 15-min than after the 45-min nap, or after no nap had been taken, while its amplitude was not affected by the length of nap. Subjective sleepiness was lower after both naps than after no nap. The task performance was significantly better during the second half of the last task session after the 15-min nap than after no nap. The high-frequency component of the R-R interval spectrum increased significantly during the 45-min nap, showing a temporary shift to a predominance of the parasympathetic nervous system. Mean total sleep times during the 15- and 45-min naps were 7.3 and 30.1 min, respectively. These results would indicate that the 15-min nap may serve to shorten the stimulus evaluation time, reducing subjective sleepiness, and slightly improving task performance. Our data demonstrated that in our subjects a brief nap after lunch was effective for enhancing subsequent alertness and performance after normal sleep the previous night.

Electroencephalographic (EEG) and heart rate (HR) responses to repeated 8-h exposure for 6 weeks to trichloroethylene (TRI) vapor of 50, 100 and 300 ppm were examined in freely moving rats with chronically implanted electrodes for polygraphic recordings. Exposure to all the TRI levels significantly decreased amount of time spent in wakefulness (W) during the exposure period. Exposure to 100 ppm and higher levels significantly decreased the time-averaged HR during the post-exposure period. The HRs during the stages of slow-wave sleep (SWS) and paradoxical sleep (PS) were significantly lowered after cessation of exposure to 50 ppm. When compared with the previously reported responses to short-term exposure to TRI (Arito H, et al. Arch Toxicol 1993; 67: 193-199), significant changes in wakefulness-sleep and HR elicited by the long-term exposure appeared at lower exposure levels. The EEG and HR effects of long-term exposure to TRI of 50 ppm or higher levels are discussed for their causative factors on the basis of the reported findings and for validity of the ongoing biological exposure limit value of TRI with reference to documentations enlisted for ACGIH's TLV of 50 ppm (ACGIH. Documentation of the threshold limit values and biological exposure indices, 5th ed. 1986: 595-597).

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.

Rats were chronically implanted with electrodes for EEG, EMG and ECG recordings and exposed to 0.1 ppm, 0.2 ppm ozone (O3) or clean air as control for 5 consecutive days. Amounts of wakefulness (W), slow-wave sleep (SWS) and paradoxical sleep (PS) of the O3-exposed rats were not statistically different from respective control values. Compared with control rats, heart rates of the O3-exposed rats decreased and the number of bradyarrhythmic episodes increased with an increase in O3 levels. The O3-induced bradyarrhythmias occurred more prevalently in the order of W, SWS and PS state. Parasympathetic mechanisms were suggested on those cardiac abnormalities.

Male rats with indwelling electrodes for electroencephalographic (EEG), electromyographic (EMG) and electrooculographic (EOG) recordings were exposed via inhalation to 900 ppm and 2700 ppm toluene vapor continuously for a 8-h period or repeatedly for 3 weeks at a rate of 8 h/day and 5 days/week. Rats exposed to a clean air-stream under the same exposure schedules served as controls. Polygraphic recordings were made on 3 consecutive days after cessation of the single 8-h and repeated 3-week exposures to 900 ppm and 2700 ppm toluene vapor or clean airstream. Amounts of time spent in wakefulness (W), slow-wave sleep (SWS) and paradoxical sleep (PS) were quantified by visual inspection of the polygraphic records. Single exposure to toluene produced a prolonged PS latency and a long-lasting increase in SWS at the expense of depressed W, whereas repeated exposures prolonged both SWS and PS latencies, abolished the initial increase of SWS and increased the light-phase level of W on Days 1 and 2. The prolonged PS latency and the decreased light-phase PS on Day 2 induced by single exposure to toluene still persisted after repeated exposures. There were no statistically significant differences in attenuation of brain and blood toluene levels between single and repeated exposures to toluene vapor of 900 ppm and 2700 ppm.

Effects of methylmercury chloride (MMC) on circadian sleep-waking rhythms were examined in rats which had been chronically implanted with EEG and EMG electrodes. Bihourly distributions of wakefulness (W), slow wave sleep (SWS) and paradoxical sleep (PS) and 12-h amounts of W, SWS and PS during light and dark periods were measured before and after MMC administration for 2 successive days at 3 dose levels. A total dose of 10 mg MMC/kg body wt was found to be the threshold for inducing reversible changes in the sleep-waking patterns. A total dose of 30 mg MMC/kg produced an increase in both dark-phase SWS and PS as well as a decrease in light-phase PS at the expense of an increase in light-phase W and a delayed phase of the circadian PS rhythm. The delayed phase of the PS rhythm tended to persist after the increased SWS during the dark period returned to normal. Brain mercury concentrations were measured in order to find the dose-response relationship and the time dependence of the MMC-induced sleep disorder. The sleep-waking disorder was found to appear at lower levels of brain Hg and shorter latency than behavioral disorders of movement and postural maintenance previously reported [5-8].