Yehuda S, Caspy T, Carasso R L
Department of Psychology, Bar-Ilan University, Ramat-Gan, Israel.
Int J Neurosci. 1988 Oct;42(3-4):259-65. doi: 10.3109/00207458808991600.
Groups of control and Area Postrema rats were treated with 0.1 mg/kg, i.p., DSIP or with saline, at 06:00, 09:00, 12:00, 15:00, 18:00, 21:00, 24:00, and at 03:00. Colonic temperature, blood pressure, and heart rate were measured 30 min after treatment. DSIP induced a shift in the hyperthermic cycle of control rats, but was unable to modify the noncyclic hypothermia found among Area Postrema-lesioned rats. Furthermore, DSIP caused a decrease in the blood pressure level of control rats, but had no such effect on the already depressed level of blood pressure in the Area Postrema-lesioned rats. Finally, DSIP decreased the heart rate of control rats and significantly antagonized the elevated heart rate observed in the Area Postrema-lesioned rats. The data do not permit us directly to relate the physiological change induced by DSIP to its sleep-promoting effects.
将对照组和最后区损毁大鼠分为若干组，于06:00、09:00、12:00、15:00、18:00、21:00、24:00及03:00腹腔注射0.1mg/kg的DSIP或生理盐水。给药30分钟后测量结肠温度、血压和心率。DSIP使对照组大鼠的体温升高周期发生偏移，但无法改变最后区损毁大鼠出现的非周期性体温过低。此外，DSIP使对照组大鼠的血压水平降低，但对最后区损毁大鼠已降低的血压水平没有此作用。最后，DSIP降低了对照组大鼠的心率，并显著对抗了最后区损毁大鼠中观察到的心率升高。这些数据不允许我们直接将DSIP诱导的生理变化与其促睡眠作用联系起来。
