Activation of the adrenocortical axis by surgical stress: Involvement of central norepinephrine and interleukin-1

Activation of the adrenocortical axis by surgical stress: Involvement of central norepinephrine and interleukin-1
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DOI:
10.1159/000026437
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发表时间:
2000-01-01
影响因子:
2.4
通讯作者:
Weidenfeld, J
Weidenfeld, J
中科院分区:
医学4区
文献类型:
--
作者:
DeKeyser, FG;Leker, RR;Weidenfeld, J

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在本研究中,我们研究了手术应激后肾上腺皮质轴激活的机制。成年雄性大鼠在乙醚麻醉下进行剖腹或开颅手术,而对照组大鼠仅进行乙醚麻醉。剖腹或开颅手术后4小时,血清促肾上腺皮质激素(ACTH)和皮质酮(CS)显著升高,24小时后几乎恢复到基础水平。剖腹手术也导致正中隆起(ME)中促肾上腺皮质激素释放激素(CRH-41)的显著耗竭。用地塞米松50 μ g/kg预处理完全消除垂体-肾上腺反应,而用II型皮质类固醇受体拮抗剂预处理引起ACTH和CS的显著高分泌,并抑制地塞米松的作用。脑室旁核(PVN)注射6-羟多巴胺可使大鼠对剖腹手术的反应明显减弱,从而使PVN中的去甲肾上腺素(NE)含量显著减少。侧脑室注射白细胞介素1受体拮抗剂(IL-1 ra)也能抑制剖腹手术引起的垂体-肾上腺反应。结果提示:(1)手术应激通过ME和NE向室旁核释放CRH激活下丘脑-垂体-肾上腺(HPA)轴;(2)肾上腺皮质反应对糖皮质激素的负反馈敏感,并通过II型糖皮质激素受体介导;(3)中枢IL-1可能是HPA轴对手术应激反应的介导者。版权所有(C)2000 S. Karger AG.巴塞尔。
In the present study, we examined the mechanisms involved in the activation of the adrenocortical axis following surgical stress. Adult male rats underwent surgical laparotomy or craniotomy under ether anesthesia while control rats were only ether-anesthetized. Four hours following laparotomy or craniotomy, serum adrenocorticotropin (ACTH) and corticosterone (CS) were significantly increased and returned to almost basal levels after 24 h. Laparotomy also caused a significant depletion of corticotropin-releasing hormone (CRH-41) in the median eminence (ME). Pretreatment with dexamethasone 50 mu g/kg completely abolished the pituitary-adrenal response while pretreatment with type II corticosteroid receptor antagonist caused a significant hypersecretion of both ACTH and CS and inhibited the effect of dexamethasone. The response to laparotomy was markedly attenuated in rats injected with 6-hydroxydopamine into the paraventricular nucleus (PVN) which significantly depletes norepinephrine (NE) PVN content. Intracerebroventricular injection of interleukin-l receptor antagonist (IL-1ra) also inhibited the pituitary-adrenal response to laparotomy. The results suggest that (1) surgical stress activates the hypothalamo-pituitary-adrenal (HPA) axis via a mechanism which involves the release of CRH from the ME and NE input to the PVN; (2) the adrenocortical response is sensitive to the negative feedback of glucocorticoids via the mediation of type II glucocorticoid receptors, and(3) central IL-1 may be a mediator in the HPA axis response to surgical stress. Copyright (C) 2000 S. Karger AG. Basel.