Endotoxin-stimulated opioid peptide secretion: two secretory pools and feedback control in vivo.
Endotoxin-stimulated opioid peptide secretion: two secretory pools and feedback control in vivo.
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DOI：
10.1126/science.6285473
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发表时间：
1982-08
期刊：
影响因子：
56.9
通讯作者：
Daniel B. Carr;Richard Bergland;Allan J. Hamilton;Howard W. Blume;Norman W. Kasting;Michael A. Arnold-Michael-A.-Arn
中科院分区：
文献类型：
--
作者：
Daniel B. Carr;Richard Bergland;Allan J. Hamilton;Howard W. Blume;Norman W. Kasting;Michael A. Arnold-Michael-A.-Arn
小剂量内毒素诱发绵羊阿片肽分泌入血的戏剧性双相反应。第一阶段在几分钟内开始，并与发热或低血压出现之前对内毒素的短暂高血压反应相一致。β-内啡肽与β-促脂素的比率在释放的第二阶段开始时突然下降，这表明富含β-内啡肽的池的早期耗尽和随后出现的富含未加工前体的池。在第二阶段，脑脊液阿片类药物的浓度增加了10倍。纳洛酮给药增加内毒素诱导的阿片类物质分泌的早期和晚期阶段，表明应激诱导的内啡肽分泌的短回路反馈调节。
Small doses of endotoxin evoked a dramatic biphasic response of opioid peptide secretion into blood in sheep. The first phase began within minutes and coincided with a brief hypertensive response to endotoxin well before the appearance of fever or hypotension. The ratio of beta-endorphin to beta-lipotropin fell abruptly at the onset of the second phase of release, suggesting early depletion of a pool rich in beta-endorphin and subsequent emergence of a pool rich in unprocessed precursor. The concentration of cerebrospinal fluid opioids increased tenfold during the second phase. Naloxone administration augmented endotoxin-induced opioid secretion in both early and late phases, suggesting a short-loop feedback regulation of stress-induced endorphin secretion.