Takagi H, Shiomi H, Kuraishi Y, Fukui K, Ueda H
Eur J Pharmacol. 1979 Feb 15;54(1-2):99-107. doi: 10.1016/0014-2999(79)90412-6.
Experiments were carried out to determine whether noxious stimulation produced biochemical changes in noradrenergic neurons in the spinal cord of rats and whether morphine induced different biochemical effects in the presence and the absence of noxious stimuli. Noxious stimuli, but not stress, significantly increased the normetanephrine (NM) concentration only in the dorsal half of the spinal cord without affecting the noradrenaline concentration. The NM increase induced by noxious stimuli remained after transection at the inter-collicular level. The NM increase induced by noxious stimuli remained after transection at the inter-collicular level. When the noxious stimulation was blocked by lidocaine at the peripheral level, the NM increase disappeared. THe NM concentration elevated by pain, was further increased by morphine. The data suggest that the bulbospinal noradrenergic system works as a pain control system: pain itself slightly activates this system, but not to the extent of producing analgesia and the addition of morphine further activates this system to a level sufficient to produce analgesia.
开展实验以确定有害刺激是否会在大鼠脊髓的去甲肾上腺素能神经元中产生生化变化,以及吗啡在有无有害刺激的情况下是否会产生不同的生化效应。有害刺激而非应激,仅在脊髓背侧显著增加了去甲变肾上腺素(NM)浓度,而不影响去甲肾上腺素浓度。有害刺激诱导的NM增加在丘间水平横断后依然存在。当有害刺激在外周水平被利多卡因阻断时,NM增加消失。疼痛引起的NM浓度升高,会因吗啡而进一步增加。数据表明,延髓脊髓去甲肾上腺素能系统作为一个疼痛控制系统发挥作用:疼痛本身会轻微激活该系统,但未达到产生镇痛作用的程度,而吗啡的加入会进一步将该系统激活至足以产生镇痛作用的水平。