Ströhle A, Holsboer F, Rupprecht R
Max Planck Institute of Psychiatry, Munich, Germany.
Neuropsychopharmacology. 2000 Mar;22(3):251-6. doi: 10.1016/S0893-133X(99)00115-3.
Preclinical findings on the role of corticotropin releasing hormone (CRH) in stress and anxiety, on the interaction of CRH and cholecystokinin (CCK) in modulating anxiety, as well as the blunted corticotropin (ACTH) response to CRH in panic disorder suggest that CRH may play a role in panic disorder. To further characterize the role of the hypothalamic-pituitary-adrenocortical (HPA) system in panic disorder, we compared patients with and without CCK tetrapeptide (CCK-4) induced panic attacks. Twenty-four patients with panic disorder were given injections of CCK-4 (25 micrograms). Panic attacks, psychopathological changes, as well as ACTH and cortisol secretion were recorded. Fifteen of the 24 patients experienced a panic attack after CCK-4. ACTH secretion was significantly higher in the patients with CCK-4-induced panic attacks than in those without such attacks. The patients without CCK-4-induced attacks had a brief but less pronounced increase in ACTH concentrations. Cortisol concentrations were not significantly increased after CCK-4 administration. The increased ACTH concentrations suggest that the activation of the HPA system in CCK-4-induced panic attacks plays a physiological role. CRH may be involved in experimentally-occurring and perhaps in naturally-occurring panic attacks as well.
促肾上腺皮质激素释放激素（CRH）在应激和焦虑中的作用、CRH与胆囊收缩素（CCK）在调节焦虑中的相互作用，以及惊恐障碍中促肾上腺皮质激素（ACTH）对CRH反应迟钝等临床前研究结果表明，CRH可能在惊恐障碍中发挥作用。为了进一步明确下丘脑-垂体-肾上腺皮质（HPA）系统在惊恐障碍中的作用，我们比较了接受和未接受CCK四肽（CCK-4）诱发惊恐发作的患者。24例惊恐障碍患者接受了CCK-4（25微克）注射。记录惊恐发作、心理病理学变化以及ACTH和皮质醇分泌情况。24例患者中有15例在注射CCK-4后出现惊恐发作。CCK-4诱发惊恐发作的患者中ACTH分泌显著高于未出现此类发作的患者。未出现CCK-4诱发发作的患者ACTH浓度有短暂但不太明显的升高。注射CCK-4后皮质醇浓度没有显著升高。ACTH浓度升高表明HPA系统在CCK-4诱发的惊恐发作中激活发挥了生理作用。CRH可能参与了实验性发生的惊恐发作，也可能参与了自然发生的惊恐发作。
