Guarini S, Rompianesi E, Ferrari W, Bertolini A
Neuropeptides. 1986 Jul;8(1):19-24. doi: 10.1016/0143-4179(86)90060-0.
ACTH-(1-24), intravenously injected at the dose of 160 micrograms/kg to rats bled to the point of otherwise irreversible hypovolemic shock, causes a prompt and sustained increase in blood pressure and pulse amplitude, all treated rats surviving at the end of the experiment (2 hr). Bilateral vagotomy, as well as atropine sulphate (2 mg/kg i.p. immediately before bleeding), almost completely abolishes the anti-shock activity of ACTH. These data indicate that a central cholinergic pathway and vagal afferent (but not efferent) fibers play an important role in the anti-shock effect of ACTH.
以160微克/千克的剂量静脉注射促肾上腺皮质激素（1 - 24）给因放血而处于即将发生不可逆性低血容量性休克状态的大鼠，会导致血压和脉搏振幅迅速且持续升高，所有接受治疗的大鼠在实验结束时（2小时）均存活。双侧迷走神经切断术以及硫酸阿托品（放血前立即腹腔注射2毫克/千克）几乎完全消除了促肾上腺皮质激素的抗休克活性。这些数据表明，中枢胆碱能通路和迷走神经传入（而非传出）纤维在促肾上腺皮质激素的抗休克作用中起重要作用。
