Naito K, Osama H, Ueno R, Hayaishi O, Honda K, Inoué S
Institute for Medical and Dental Engineering, Tokyo Medical and Dental University, Japan.
Brain Res. 1988 Jun 21;453(1-2):329-36. doi: 10.1016/0006-8993(88)90173-4.
Sleep-suppressive activity of prostaglandin synthesis inhibitors, diclofenac sodium (DF) and indomethacin (IM), was examined in unrestrained male rats. An intraperitoneal injection of 5 mg/kg IM, or an oral administration of 5 mg/kg DF and 10 mg/kg IM at an early phase of the light period transiently decreased slow wave sleep (SWS) and paradoxical sleep (PS) to 30-62% and 0-38%, respectively, of the control level in the first hour. An intravenous infusion of 0.4 mg DF or 0.4 mg IM or an intracerebroventricular infusion of 0.04 mg DF continuously during a 10-h diurnal period resulted in a significant decrease in SWS and PS by 9-17% and 17-21%, respectively, from the baseline value in the 12-h light period. The DF infusion was accompanied by a rebound rise in the nocturnal SWS and PS and the subsequent diurnal PS. The results indicate that the depletion of prostaglandin(s) in the brain is responsible for the DF- and IM-induced suppression of sleep.
在自由活动的雄性大鼠中检测了前列腺素合成抑制剂双氯芬酸钠（DF）和吲哚美辛（IM）的睡眠抑制活性。在光照期早期腹腔注射5mg/kg的IM，或口服5mg/kg的DF和10mg/kg的IM，在第一小时内可使慢波睡眠（SWS）和异相睡眠（PS）分别短暂降至对照水平的30%-62%和0%-38%。在10小时的白天期间持续静脉输注0.4mg的DF或0.4mg的IM，或脑室内输注0.04mg的DF，导致SWS和PS分别比12小时光照期的基线值显著降低9%-17%和17%-21%。DF输注伴随着夜间SWS和PS以及随后白天PS的反弹升高。结果表明，脑内前列腺素的耗竭是DF和IM诱导睡眠抑制的原因。
