Guarini S, Vergoni A V, Bertolini A
Pharmacol Res Commun. 1987 Mar;19(3):255-60. doi: 10.1016/0031-6989(87)90068-3.
In an experimental model of hypovolemic shock in rats, produced by withdrawing about 50% of the estimated total blood volume, and causing 100% deaths within 30 min, ACTH-(1-24) dose-dependently improved arterial and pulse pressure and increased survival rate. The intracerebroventricular (i.c.v.) route of administration was more effective than the intravenous (i.v.) route: at the dose of 24 micrograms/kg, 45% and 91% of rats were still surviving 2 hr after i.v. and i.c.v. treatment, respectively. At higher doses of ACTH-(1-24), the survival rate rose to 100% regardless of the route of administration, but arterial pressure increased more after i.c.v. than after i.v. injection. These data suggest that the CNS plays an important role in the anti-shock effect of ACTH.
在通过抽取约50%估计总血容量建立的大鼠低血容量性休克实验模型中，该模型会在30分钟内导致100%死亡，促肾上腺皮质激素（1-24）[ACTH-(1-24)]呈剂量依赖性地改善动脉压和脉压，并提高存活率。脑室内（i.c.v.）给药途径比静脉内（i.v.）给药途径更有效：在24微克/千克的剂量下，静脉内和脑室内给药治疗后2小时，分别有45%和91%的大鼠存活。在更高剂量的ACTH-(1-24)下，无论给药途径如何，存活率均升至100%，但脑室内注射后动脉压的升高幅度大于静脉内注射。这些数据表明，中枢神经系统在ACTH的抗休克作用中起重要作用。
