Inhibition of the adrenocorticotropin and corticosteroid responses to hypoglycemia after prior stress.

Inhibition of the adrenocorticotropin and corticosteroid responses to hypoglycemia after prior stress.
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DOI:
10.1210/endo-113-2-491
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发表时间:
1983-08
期刊:
影响因子:
4.8
通讯作者:
M. Keller‐Wood;J. Shinsako;M. Dallman
M. Keller‐Wood;J. Shinsako;M. Dallman
中科院分区:
医学2区
文献类型:
--
作者:
M. Keller‐Wood;J. Shinsako;M. Dallman

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我们已经测试了先前应激诱导的皮质类固醇增加对2小时后诱导的低血糖的ACTH反应的抑制的功效。在五个实验中的每一个中研究了五只狗。在每个实验中,有两个刺激期;在第一个刺激期中,给予5%葡萄糖、3或10微克/kg × min硝普钠或0.05或0.10 U/kg胰岛素,在第二个刺激期中,给予0.10 U/kg胰岛素。而先前输注5%葡萄糖并不影响随后的ACTH反应0.10 U/kg胰岛素,垂体-肾上腺轴的先前刺激对随后的ACTH反应0.10 U/kg胰岛素有显着的影响。通过10 μ g/kg/min硝普钠或0.10 U/kg胰岛素的预先刺激,对低血糖的综合ACTH反应显著降低,尽管在第二次刺激期间低血糖的强度没有被任何预先刺激改变。总体而言,垂体-肾上腺对低血糖反应的抑制程度与第一次刺激产生的血浆皮质类固醇增加显著相关,并且与先前研究中观察到的ACTH或皮质类固醇输注后皮质类固醇反馈抑制ACTH的程度一致。因此,我们的结论是,先前的刺激下丘脑-垂体-肾上腺轴的清醒的狗低血压或低血糖抑制随后的反应成比例的皮质类固醇反馈信号产生。
We have tested the efficacy of prior stress-induced increases in corticosteroids on inhibition of the ACTH response to hypoglycemia induced 2 h later. Five dogs were studied in each of five experiments. In each experiment, there were two stimulus periods; in the first, 5% dextrose, 3 or 10 micrograms/kg X min nitroprusside, or 0.05 or 0.10 U/kg insulin was administered, and in the second, 0.10 U/kg insulin was administered. Whereas prior infusion of 5% dextrose did not affect the subsequent ACTH response to 0.10 U/kg insulin, prior stimulation of the pituitary-adrenal axis had a significant effect on the subsequent ACTH response to 0.10 U/kg insulin. The integrated ACTH response to hypoglycemia was significantly reduced by prior stimulation by either 10 micrograms/kg/min nitroprusside or 0.10 U/kg insulin, although the intensity of the hypoglycemia during the second stimulus period was not altered by any of the prior stimuli. Overall, the magnitude of the suppression of the pituitary-adrenal response to hypoglycemia was significantly related to the increase in plasma corticosteroids produced by the first stimulus, and was consistent with the degree of corticosteroid feedback inhibition of ACTH observed in previous studies after ACTH or corticosteroid infusion. Therefore, we conclude that prior stimulation of the hypothalamo-pituitary-adrenal axis of conscious dogs by hypotension or hypoglycemia inhibits subsequent responses in proportion to the corticosteroid feedback signal produced.