LaHann T R, Horita A
J Pharmacol Exp Ther. 1982 Jul;222(1):66-70.
The central, but not the peripheral, administration of thyrotropin releasing hormone (TRH) elicited an increase in the gastrointestinal (GI) motor activity in anesthetized rabbits. This effect did not appear to be mediated via the pituitary-thyroid axis and it was relatively independent of the degree of basal motor activity in the Gl tract. Intravenous administration of either atropine or ganglionic blocking agents antagonized this phenomenon. Bilateral vagal transection prevented the TRH-induced stimulation of Gl motor activity, but neither spinal transection nor i.v. guanethidine had any effect. When injected into the lateral ventricles, 3rd ventricle of cisterna magna, TRH always elicited its Gl effects. Central cholinergic mechanisms appear to be involved because both atropine methyl bromide and atropine sulfate given i.c.v. antagonized the Gl effects. Intravenous injection of phenoxybenzamine also inhibited the TRH effect. TRH stimulates neural pathways within the central nervous system to activate efferent vagal fibers leading to a generalized increase in the motor activity of the Gl tract.
促甲状腺激素释放激素(TRH)经中枢而非外周给药可引起麻醉兔胃肠道(GI)运动活性增加。这种效应似乎并非通过垂体-甲状腺轴介导,且相对独立于胃肠道基础运动活性的程度。静脉注射阿托品或神经节阻断剂可拮抗此现象。双侧迷走神经切断可阻止TRH诱导的胃肠道运动活性刺激,但脊髓切断或静脉注射胍乙啶均无任何作用。当注入侧脑室、第三脑室或小脑延髓池时,TRH总能引发其对胃肠道的效应。中枢胆碱能机制似乎参与其中,因为腹腔注射甲基溴阿托品和硫酸阿托品均可拮抗对胃肠道的效应。静脉注射酚苄明也可抑制TRH的效应。TRH刺激中枢神经系统内的神经通路,激活传出迷走神经纤维,导致胃肠道运动活性普遍增加。