Neuroendocrine responses to psychological stress in adolescents with anxiety disorder
Neuroendocrine responses to psychological stress in adolescents with anxiety disorder
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DOI：
10.1159/000026677
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发表时间：
2000-01-01
影响因子：
3.2
通讯作者：
Brambilla, F
中科院分区：
文献类型：
--
作者：
Gerra, G;Zaimovic, A;Brambilla, F
采用心理压力混合模型测试（心算、Stroop彩色单词干扰任务、Trier社会压力测试）对20例青春期焦虑障碍男性受试者（a组）的神经递质-神经内分泌和心血管反应进行了研究。14名广泛性焦虑障碍患者，6名广泛性焦虑障碍和分离性焦虑障碍患者)和20名初中生，年龄匹配，无明显心理障碍（B组）。在试验开始前和试验结束后30分钟分别测定血浆中去甲肾上腺素（NE）、肾上腺素（EPI）、促肾上腺皮质激素（ACTH）、β -内啡肽（β - ep）、皮质醇（CORT）、生长激素（GH）、催乳素（PRL）和睾酮（Te）的水平。焦虑组GH、PRL、β - ep和ACTH的平均预应力值显著高于对照组。两组患者的NE、EPI、心血管CORT和血压水平均无差异。在心理应激期后，焦虑受试者的NE、GH和Te浓度显著增加(A)，而对照组没有。相比之下，焦虑被试的β - ep和PRL在心理应激过程中显著下降，而非焦虑被试的β - ep和PRL在应激过程中不受影响。在挑战过程中，焦虑组和对照组的ACTH、CORT和EPI均未发生显著变化，这可能与应激后采血时间较晚有关。与对照组相比，在心理压力测试后，焦虑受试者的心率和收缩压显著升高。我们的数据支持这样的假设，即应激反应中去甲肾上腺素能系统的过度活跃与青少年焦虑症有关，并可能影响GH和Te的反应。在焦虑受试者中，压力激素的基础值似乎是由对任务的预期或去甲肾上腺素能系统的持续过度活跃引起的。进一步的研究需要通过更精确的血液采样时间点来更详细地调查焦虑青少年中下丘脑轴的参与。版权所有(C) 2000 S. Karger AG，巴塞尔。
Neurotransmitter-neuroendocrine and cardiovascular responses to the administration of a psychologically stressful mixed-model test (Mental Arithmetic, Stroop Color Word Interference Task, Trier Social Stress Test) were examined in 20 male peripubertal subjects affected by anxiety disorder (group A: 14 with generalized anxiety disorder, 6 with generalized anxiety disorder and separation anxiety disorder) and 20 junior school adolescents, matched for age, without overt psychological disorders (group B). Plasma levels of norepinephrine (NE), epinephrine (EPI), adrenocorticotropic hormone (ACTH), beta-endorphin (beta-EP), cortisol (CORT), growth hormone (GH), prolactin (PRL) and testosterone (Te) were measured immediately before the beginning of the tests and 30 min later at their end. Mean prestress values of GH, PRL, beta-EP and ACTH were significantly higher in anxious subjects than in controls. There was no difference in NE, EPI, cardiovascular CORT and Te prestress levels in the two groups. After the psychological stress session NE, GH and Te concentrations increased significantly in anxious subjects (A), but not in controls. In contrast, beta-EP and PRL decreased significantly during the psychological stress session in anxious subjects, and were unaffected by stress in the subjects without anxiety. No significant changes were found in ACTH, CORT and EPI during the challenge either in anxious subjects or in controls, which may be attributed to the late time of poststress blood sampling. In contrast to controls, heart rate and systolic blood pressure increased significantly in anxious subjects after psychological stress testing. Our data support the hypothesis that the hyperactivity of the noradrenergic system in response to stress is associated with anxiety disorders in adolescents and might influence the responses of GH and Te. High prestress basal values of stress hormones seem to be induced in anxious subjects by the anticipation of the task or by a persistent hyperactivity of the noradrenergic system. Further studies are needed to investigate in more detail the involvement of the HPA axis in anxious adolescents by a more refined resolution of time points of blood sampling. Copyright (C) 2000 S. Karger AG, Basel.