FORENAP, Rouffach, France.
J Psychopharmacol. 2011 Jan;25(1):52-9. doi: 10.1177/0269881110367449. Epub 2010 May 24.
Benzodiazepine effects on cholecystokinin tetrapeptide (CCK-4)-induced panic attack (PA) in humans are incompletely characterized, in particular on the neurofunctional level. This work explores the effects of lorazepam on brain activity and behavioral and physiological symptoms related to CCK-4-induced PA in healthy volunteers. Twenty-one male volunteers received 1 mg of lorazepam or placebo orally, 2 hours before an injection of 0.9% saline solution followed by 50 µg of CCK-4 during functional magnetic resonance imaging (fMRI) and heart rate recording. Panic attacks were defined using the panic symptom scale (PSS). In addition, the Y1-STAI (state anxiety) and the Bond & Lader Visual Analogue Scale (VAS) were used. Eleven subjects were classified as panickers. CCK-4 induced behavioral anxiety and cardiovascular effects along with cerebral activation in anxiety-related brain regions. Overall, lorazepam did not significantly modify the anxiogenic and cardiovascular effects of CCK-4. Regarding CCK-4-induced brain activation, lorazepam did not reduce activity in the insulae and cingulate gyrus of panickers. One milligram of lorazepam was not sufficient to reverse strong panicogenic effects, but decreased brain activity in the case of mild anxiety.
苯二氮䓬类药物对人体胆囊收缩素四肽（CCK-4）诱发的惊恐发作（PA）的影响尚未完全确定，特别是在神经功能水平上。本研究旨在探讨劳拉西泮对健康志愿者 CCK-4 诱导的 PA 相关脑活动、行为和生理症状的影响。21 名男性志愿者在接受 0.9%生理盐水注射后 2 小时口服 1mg 劳拉西泮或安慰剂，随后在功能磁共振成像（fMRI）和心率记录期间给予 50μg CCK-4。惊恐发作使用惊恐症状量表（PSS）定义。此外，还使用了 Y1-STAI（状态焦虑）和邦德和莱德视觉模拟量表（VAS）。11 名受试者被归类为惊恐发作者。CCK-4 引起了行为焦虑和心血管效应，以及与焦虑相关的大脑区域的脑激活。总体而言，劳拉西泮并未显著改变 CCK-4 的焦虑和心血管效应。关于 CCK-4 诱导的脑激活，劳拉西泮并未降低惊恐发作者的岛叶和扣带回 gyrus 的活动。1mg 劳拉西泮不足以逆转强烈的惊恐发作效应，但在轻度焦虑的情况下会降低大脑活动。
