Franklin K B, Kelly S J
Eur J Pharmacol. 1986 Jul 15;126(1-2):145-50. doi: 10.1016/0014-2999(86)90751-x.
Guanethidine treatment decreased morphine analgesia exhibited by restrained rats but had no effect on morphine analgesia exhibited by unrestrained rats or on baseline pain sensitivity. Guanethidine also prevented the rise in tryptophan uptake into the brain induced by the restraint stress. It is argued that the prevention of the stress-induced increase in brain tryptophan uptake is causal to guanethidine's attenuation of morphine analgesia exhibited by restrained rats, since the increase in brain tryptophan uptake has already been shown to be critical to this phenomenon. The blockade of the stress-induced increase in brain tryptophan uptake and morphine analgesia by guanethidine support the hypothesis that these effects depend upon sympathetic activity.
胍乙啶治疗降低了受束缚大鼠所表现出的吗啡镇痛效果，但对未受束缚大鼠所表现出的吗啡镇痛效果或基线疼痛敏感性没有影响。胍乙啶还阻止了束缚应激诱导的大脑中色氨酸摄取量的增加。有人认为，阻止应激诱导的大脑色氨酸摄取量增加是胍乙啶减弱受束缚大鼠所表现出的吗啡镇痛效果的原因，因为大脑色氨酸摄取量的增加已被证明对这一现象至关重要。胍乙啶对应激诱导的大脑色氨酸摄取量增加和吗啡镇痛效果的阻断支持了这些作用依赖于交感神经活动的假说。
