Vergoni A V, Marrama D, Guarini S, Tagliavini S, Bazzani C, Maugeri A, Bertolini A
Institute of Pharmacology, University of Modena, Italy.
Pharmacol Res. 1991 Apr;23(3):271-8. doi: 10.1016/s1043-6618(05)80086-6.
In a model of haemorrhagic shock causing the death of all saline-treated rats within 25.8 +/- 2.7 min after treatment, the intravenous injection of thyrotropin-releasing hormone tartrate (TRH-T) at the dose of 4 mg/kg induces a prompt and sustained increase of arterial pressure and pulse amplitude, with survival of all rats. Bilateral vagotomy, atropine sulphate (2 mg/kg intraperitoneally) and hemicholinium-3 (20 micrograms/rat intracerebroventricularly) partially prevent the TRH-T-induced shock reversal, whereas atropine methylbromide has no effect. These data indicate that afferent vagal fibres, brain cholinergic neurons and central muscarinic receptors play a role in the mechanism of the anti-shock effect of TRH-T.
在失血性休克模型中，所有接受生理盐水治疗的大鼠在治疗后25.8±2.7分钟内死亡，静脉注射剂量为4mg/kg的酒石酸促甲状腺激素释放激素（TRH-T）可使动脉压和脉搏幅度迅速且持续升高，所有大鼠均存活。双侧迷走神经切断术、硫酸阿托品（腹腔注射2mg/kg）和半胱氨酸-3（脑室内注射20μg/大鼠）可部分阻止TRH-T诱导的休克逆转，而甲基溴化阿托品则无作用。这些数据表明，迷走神经传入纤维、脑胆碱能神经元和中枢毒蕈碱受体在TRH-T抗休克作用机制中发挥作用。
