神经元和血管钙通道在促肾上腺皮质激素诱导的失血性休克逆转中的作用。
Role of neuronal and vascular Ca(2+)-channels in the ACTH-induced reversal of haemorrhagic shock.
作者信息
Guarini S, Bazzani C, Bertolini A
机构信息
Institute of Pharmacology, University of Modena, Italy.
出版信息
Br J Pharmacol. 1993 Jul;109(3):645-50. doi: 10.1111/j.1476-5381.1993.tb13621.x.
Abstract
- In a rat model of volume-controlled haemorrhagic shock causing the death of all control (saline-treated) animals within 30 min, the intravenous (i.v.) bolus injection of ACTH-(1-24) at a dose of 160 micrograms kg-1 produced an impressive and sustained restoration of arterial pressure, pulse pressure and respiratory function, with 100% survival at the end of the observation period (2 h). 2. Both intracerebroventricular (i.c.v., 0.015-0.06 microgram kg-1) and i.v. (5 micrograms kg-1) pretreatment with the N-calcium channel blocker, omega-conotoxin GVIA, and i.v. (but not i.c.v.) pretreatment with the L-calcium channel blocker, nicardipine (125-500 micrograms kg-1) dose-dependently prevented the ACTH-induced shock reversal. 3. These results further indicate that the effect of ACTH in haemorrhagic shock may involve a neuronal link and the eventual restoration of vascular tone mediated by N- and L-type calcium channels, respectively.
摘要
- 在容量控制型失血性休克大鼠模型中，所有对照（生理盐水处理）动物在30分钟内死亡，静脉推注剂量为160微克/千克的促肾上腺皮质激素（1-24）可显著且持续地恢复动脉压、脉压和呼吸功能，在观察期（2小时）结束时存活率达100%。2. 用N型钙通道阻滞剂ω-芋螺毒素GVIA进行脑室内（0.015-0.06微克/千克）和静脉内（5微克/千克）预处理，以及用L型钙通道阻滞剂尼卡地平（125-500微克/千克）进行静脉内（而非脑室内）预处理，均剂量依赖性地阻止了促肾上腺皮质激素诱导的休克逆转。3. 这些结果进一步表明，促肾上腺皮质激素在失血性休克中的作用可能涉及神经元联系，以及分别由N型和L型钙通道介导的血管张力的最终恢复。
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