Concentrations of corticotropin-releasing hormone, norepinephrine, MHPG, 5-hydroxyindoleacetic acid, and tryptophan in the cerebrospinal fluid of alcoholic patients: serial sampling studies.
Concentrations of corticotropin-releasing hormone, norepinephrine, MHPG, 5-hydroxyindoleacetic acid, and tryptophan in the cerebrospinal fluid of alcoholic patients: serial sampling studies.
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酒精患者脑脊液中促肾上腺皮质激素释放激素、去甲肾上腺素、MHPG、5-羟基吲哚乙酸和色氨酸的浓度：系列抽样研究。
DOI：
10.1159/000126807
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发表时间：
1994
影响因子：
4.1
通讯作者：
Orth,DN
中科院分区：
文献类型：
--
作者：
GeraciotiJr,TD;Loosen,PT;Ebert,MH;Ekhator,NN;Burns,D;Nicholson,WE;Orth,DN
在促肾上腺皮质激素释放激素（CRH）的分泌，去甲肾上腺素能神经传递，并在中枢神经系统（CNS）的肾上腺素能活动的ababandonis都被假设存在于酒精中毒患者，因为有异常的下丘脑-垂体-肾上腺功能。为了验证这些假设，我们连续采集戒酒38-124天的酒精中毒患者和正常志愿者的脑脊液（CSF），通过柔性的、留置的腰椎蛛网膜下腔导管，从11：00到17：00，每隔10分钟测量CRH、去甲肾上腺素（NE）、3-甲氧基-4-羟基苯乙二醇（MHPG）、色氨酸和5-羟基吲哚乙酸（5-HIAA）的浓度。在大约08：00时插入椎管导管。系列血浆促肾上腺皮质激素，皮质醇和NE浓度也进行了测量。在13：00 h消耗混合液体膳食。酒精中毒患者的CSF CRH浓度低于正常志愿者（分别为26 ± 15 vs. 60 ± 30 pg/ml，通过ANOVA，p < 0.05），CSF NE水平也是如此（分别为0.33 ± 0.09 vs. 1.15 ± 0.51 pmol/ml，p < 0.01）。酒精中毒患者血浆NE和CSF MHPG水平正常。CSF色氨酸和5-HIAA以及血浆ACTH和皮质醇浓度在两组之间没有差异。这些研究扩展了我们在抑郁症患者椎管内脑脊液CRH浓度降低的发现，使之适用于戒酒的慢性酗酒者。在我们的酒精患者中观察到的非常低的CSF NE水平与我们先前在抑郁症患者中发现的正常CSF NE浓度以及他们自己的血浆NE和CSF MHPG的正常水平（这在很大程度上反映了外周NE代谢）相反。脑脊液中NE和CRH浓度的不足是否是酗酒或戒酒的原因或后果，或者与酒精在酗酒者中的积极强化作用有关，仍有待确定。
Abnormalities in corticotropin-releasing hormone (CRH) secretion, noradrenergic neurotransmission, and serotonergic activity in the central nervous system (CNS) have all been hypothesized to exist in alcoholic patients, as have abnormalities in hypothalamic-pituitary adrenal function. To test these hypotheses, we continuously sampled cerebrospinal fluid (CSF) from alcoholic patients after 38-124 days of abstinence and from normal volunteers via a flexible, indwelling lumbar subarachnoid catheter and measured CRH, norepinephrine (NE), 3-methoxy-4-hydroxyphenylglycol (MHPG), tryptophan, and 5-hydroxyindoleacetic acid (5-HIAA) concentrations at 10-min intervals, from 11:00 through 17:00 h. The spinal canal catheter was inserted at approximately 08:00 h. Serial plasma ACTH, cortisol, and NE concentrations were also measured. A mixed liquid meal was consumed at 13:00 h. CSF CRH concentrations were lower in alcoholic patients than in normal volunteers (26 ± 15 vs. 60 ± 30 pg/ml, respectively, p < 0.05 by ANOVA), as were CSF NE levels (0.33 ± 0.09 vs. 1.15 ± 0.51 pmol/ml, respectively, p < 0.01). Plasma NE and CSF MHPG levels were normal in the alcoholic patients. CSF tryptophan and 5-HIAA and plasma ACTH and cortisol concentrations did not differ between the groups. These studies extend our finding of reduced spinal canal CSF CRH concentrations in depressed patients to abstinent chronic alcoholics. The very low CSF NE levels observed in our alcoholic patients stand in contrast to the normal CSF NE concentrations we previously found in depressed patients, and to their own normal levels of plasma NE and CSF MHPG (which largely reflect peripheral NE metabolism). Whether the deficits in CSF NE and CRH concentrations are the cause or consequence of alcoholism or abstinence or are related to the positively reinforcing effect of alcohol in alcoholics remains to be determined.