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在人类中,应激而非促肾上腺皮质激素释放激素诱导的垂体-肾上腺轴激活被阿普唑仑阻断。

The stress-, but not corticotropin-releasing hormone-induced activation of the pituitary-adrenal axis in man is blocked by alprazolam.

作者信息

Rohrer T, von Richthofen V, Schulz C, Beyer J, Lehnert H

机构信息

III. Medizinische Klinik, Innere Medizin-Endokrinologie, Universitätsklinik Mainz, Germany.

出版信息

Horm Metab Res. 1994 Apr;26(4):200-6. doi: 10.1055/s-2007-1000811.

Abstract

A number of experimental studies clearly suggest that benzodiazepines attenuate the corticotropin-releasing hormone (CRH) secretion possibly through inhibitory GABAergic neurons. There is some evidence that benzodiazepines act to inhibit stress-induced activation of the hypothalamic-pituitary-adrenal axis. A comparison of the effects of a benzodiazepine on the stress- and CRH-induced activation in man has not been undertaken so far. We thus investigated the effects of the triazolobenzodiazepine alprazolam on both the stress- and CRH-induced changes in ACTH, cortisol, and prolactin secretion in ten healthy volunteers. In addition, hemodynamic parameters were studied. The subjects received either alprazolam (0.5 mg orally) or placebo 90 min prior to administration of CRH (100 ug i.v.) and to the performance of a mental stress technique. Blood samples, blood pressure and heart rate were taken every 15 min. The administration of alprazolam led to a highly significant attenuation of the ACTH increase following the stress interview. While ACTH increased from 12.4 to 26.7 pg/ml 15 min after the stress procedure in the placebo condition, there was almost no increase following alprazolam intake. An identical effect was found for cortisol secretion. Basal levels of prolactin were slightly enhanced in the alprazolam situation, while the stress-induced increase was not attenuated. Basal and stimulated systolic and diastolic blood pressure levels and heart rate were also significantly attenuated by alprazolam intake. Following administration of CRH, the ACTH augmentation was only slightly affected following alprazolam, while there were no changes in cortisol and prolactin secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

多项实验研究明确表明,苯二氮䓬类药物可能通过抑制性γ-氨基丁酸能神经元来减弱促肾上腺皮质激素释放激素(CRH)的分泌。有证据表明,苯二氮䓬类药物可抑制应激诱导的下丘脑-垂体-肾上腺轴的激活。到目前为止,尚未对苯二氮䓬类药物对人体应激和CRH诱导激活的影响进行比较。因此,我们研究了三唑苯二氮䓬阿普唑仑对10名健康志愿者应激和CRH诱导的促肾上腺皮质激素(ACTH)、皮质醇和催乳素分泌变化的影响。此外,还研究了血流动力学参数。受试者在静脉注射CRH(100μg)和进行精神应激技术前90分钟,口服阿普唑仑(0.5mg)或安慰剂。每15分钟采集一次血样、测量血压和心率。服用阿普唑仑导致应激访谈后ACTH升高显著减弱。在安慰剂组中,应激程序后15分钟ACTH从12.4pg/ml增加到26.7pg/ml,而服用阿普唑仑后几乎没有增加。皮质醇分泌也有相同的效果。在阿普唑仑组中,催乳素的基础水平略有升高,而应激诱导的升高并未减弱。服用阿普唑仑后,基础和刺激后的收缩压、舒张压水平及心率也显著降低。注射CRH后,阿普唑仑对ACTH增加的影响较小,而皮质醇和催乳素分泌没有变化。(摘要截短至250字)

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