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乳酸诱导惊恐发作时垂体肾上腺皮质反应迟钝

Pituitary adrenocortical unresponsiveness in lactate-induced panic.

作者信息

Levin A P, Doran A R, Liebowitz M R, Fyer A J, Gorman J M, Klein D F, Paul S M

出版信息

Psychiatry Res. 1987 May;21(1):23-32. doi: 10.1016/0165-1781(87)90058-8.

Abstract

The hypothalamic-pituitary adrenal (HPA) axis responds to a variety of physical and emotional stimuli with increased output of adrenocorticotropic hormone (ACTH) and cortisol, yet there is little known about the activity of this system during episodes of severe anxiety in patients with DSM-III-defined anxiety disorders. To explore further whether alterations of the HPA axis occur during various anxiety states, we measured ACTH and cortisol during lactate infusion in patients with panic disorder and agoraphobia. In eight patients who panicked during lactate infusion, there were no elevations in either ACTH or cortisol. Further, the patterns of hormone secretion did not differ among patients who panicked, nonpanicking patients, or controls. This negative result suggests that the neurobiological mechanisms that mediate panic differ from those responsible for other fear responses.

摘要

下丘脑 - 垂体 - 肾上腺(HPA)轴会对各种身体和情绪刺激作出反应,增加促肾上腺皮质激素(ACTH)和皮质醇的分泌量,但对于符合《精神疾病诊断与统计手册》第三版(DSM - III)定义的焦虑症患者在严重焦虑发作期间该系统的活动情况,我们却知之甚少。为了进一步探究在各种焦虑状态下HPA轴是否会发生改变,我们对惊恐障碍和广场恐惧症患者在输注乳酸期间的促肾上腺皮质激素和皮质醇进行了测量。在8名在输注乳酸期间出现惊恐发作的患者中,促肾上腺皮质激素和皮质醇均未升高。此外,惊恐发作的患者、未发作的患者和对照组之间的激素分泌模式并无差异。这一阴性结果表明,介导惊恐发作的神经生物学机制与引发其他恐惧反应的机制不同。

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