Shiromani P J, Siegel J M, Tomaszewski K S, McGinty D J
Exp Neurol. 1986 Feb;91(2):285-92. doi: 10.1016/0014-4886(86)90069-5.
Infusions of cholinomimetics, either systemically in normal humans, or directly into the brain stem of unanesthetized cats and rats, readily induce rapid eye-movement (REM) sleep. In anesthetized cats and rats, infusions of cholinomimetics have been shown to produce both increases and decreases in arterial blood pressure. We determined the relation of these blood pressure changes to REM sleep, by examining both blood pressure and sleep states after injecting carbachol at midbrain, pontine, and medullary sites in unanesthetized cats. In the pons, carbachol infusions produced an early decrease in blood pressure followed by a sustained hypertensive effect. The early blood pressure decrease was associated with the occurrence of REM sleep; however, higher values were associated with later REM sleep episodes. In other brain stem sites carbachol did not produce REM sleep or its associated reductions in blood pressure. Instead it produced a hypertensive response that increased throughout the 1-h observation period. We hypothesize that pontine muscarinic mechanisms trigger REM sleep and a REM sleep-associated decrease in blood pressure. Thereafter, nicotinic receptors mediating the blood pressure increase override the muscarinic-induced decrease.
在正常人体内全身性注射拟胆碱药,或直接向未麻醉的猫和大鼠的脑干注射拟胆碱药,都很容易诱发快速眼动(REM)睡眠。在麻醉的猫和大鼠中,已证明注射拟胆碱药会使动脉血压升高或降低。我们通过检查未麻醉猫的中脑、脑桥和延髓部位注射卡巴胆碱后的血压和睡眠状态,来确定这些血压变化与REM睡眠的关系。在脑桥,注射卡巴胆碱会使血压先下降,随后出现持续的高血压效应。早期血压下降与REM睡眠的出现有关;然而,较高的血压值与后期的REM睡眠发作有关。在脑干的其他部位,卡巴胆碱不会产生REM睡眠或其相关的血压降低。相反,它会产生一种高血压反应,在1小时的观察期内持续增强。我们推测,脑桥毒蕈碱机制触发REM睡眠和与REM睡眠相关的血压降低。此后,介导血压升高的烟碱受体作用超过了毒蕈碱诱导的血压降低作用。