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惊恐发作会激活下丘脑-垂体-肾上腺轴吗?

Does the panic attack activate the hypothalamic-pituitary-adrenal axis?

作者信息

Graeff Frederico G, Garcia-Leal Cybele, Del-Ben Cristina M, Guimarães Francisco S

机构信息

Departmento de Neurologia, Psiquiatria e Psicologia Médica, Hospital das Clínicas da Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP 14048-900, Brazil.

出版信息

An Acad Bras Cienc. 2005 Sep;77(3):477-91. doi: 10.1590/s0001-37652005000300009. Epub 2005 Aug 24.

DOI:10.1590/s0001-37652005000300009
PMID:16127553
Abstract

A bibliographic search has been performed in MEDLINE using cortisol and panic as key-words, occurring in the title and/or in the abstract. Human studies were selected, with no time limit. The following publications were excluded: review articles, case reports, panic attacks in disorders other than panic disorder, and studies on changes that occurred in-between panic attacks. The results showed that real-life panic attacks as well as those induced by selective panicogenic agents such as lactate and carbon dioxide do not activate the hypothalamic-pituitary-adrenal (HPA) axis. Agonists of the colecystokinin receptor B, such as the colecystokinin-4 peptide and pentagastrin, increase stress hormones regardless of the occurrence of a panic attack and thus, seem to activate the HPA axis directly. The benzodiazepine antagonist flumazenil does not increase stress hormones, but this agent does not reliably induce panic attacks. Pharmacological agents that increased anxiety in both normal subjects and panic patients raised stress hormone levels; among them are the alpha2-adrenergic antagonist yohimbine, the serotonergic agents 1-(m-chlorophenyl) piperazine (mCPP) and fenfluramine, as well as the psychostimulant agent caffeine. Therefore, the panic attack does not seem to activate the HPAaxis, in contrast to anticipatory anxiety.

摘要

我们以“皮质醇”和“惊恐”作为关键词,在MEDLINE中进行了文献检索,关键词出现在标题和/或摘要中。我们选择了无时间限制的人体研究。以下出版物被排除在外:综述文章、病例报告、惊恐障碍以外的其他疾病中的惊恐发作,以及关于惊恐发作期间发生变化的研究。结果表明,现实生活中的惊恐发作以及由选择性惊恐诱发剂(如乳酸盐和二氧化碳)诱发的惊恐发作不会激活下丘脑-垂体-肾上腺(HPA)轴。胆囊收缩素受体B的激动剂,如胆囊收缩素-4肽和五肽胃泌素,无论是否发生惊恐发作都会增加应激激素,因此似乎直接激活了HPA轴。苯二氮䓬拮抗剂氟马西尼不会增加应激激素,但这种药物不能可靠地诱发惊恐发作。在正常受试者和惊恐症患者中增加焦虑的药物会提高应激激素水平;其中包括α2肾上腺素能拮抗剂育亨宾、血清素能药物1-(间氯苯基)哌嗪(mCPP)和芬氟拉明,以及精神兴奋剂咖啡因。因此,与预期性焦虑相反,惊恐发作似乎不会激活HPA轴。

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