Charney D S, Heninger G R
Arch Gen Psychiatry. 1985 May;42(5):458-67. doi: 10.1001/archpsyc.1985.01790280040004.
There is preclinical and clinical evidence suggesting that one neural mechanism responsible for antipanic efficacy is a reduction in brain noradrenergic function. Alprazolam, a triazolobenzodiazepine, has been demonstrated to have antipanic properties; however, to our knowledge, its effects on noradrenergic function have not been established. To assess whether alprazolam alters noradrenergic function, the effects of alprazolam on baseline plasma free 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG), and yohimbine-induced increases in plasma MHPG level, anxiety-nervousness, blood pressure, and somatic symptoms were studied in 14 patients with agoraphobia and panic disorder. Long-term alprazolam treatment significantly reduced plasma MHPG baseline and blunted the yohimbine-induced increases in plasma MHPG, anxiety-nervousness, and sitting systolic blood pressure. These observations suggest that the antipanic mechanism of action of alprazolam may be due in part to an interaction between benzodiazepine-sensitive and noradrenergic neural systems.
临床前和临床证据表明,一种负责抗惊恐疗效的神经机制是脑去甲肾上腺素能功能的降低。阿普唑仑是一种三唑并苯二氮䓬类药物,已被证明具有抗惊恐特性;然而,据我们所知,其对去甲肾上腺素能功能的影响尚未明确。为了评估阿普唑仑是否会改变去甲肾上腺素能功能,我们对14名患有广场恐惧症和惊恐障碍的患者进行了研究,观察阿普唑仑对基线血浆游离3-甲氧基-4-羟基苯乙二醇(MHPG)的影响,以及育亨宾引起的血浆MHPG水平、焦虑-紧张、血压和躯体症状的升高。长期阿普唑仑治疗显著降低了血浆MHPG基线水平,并减弱了育亨宾引起的血浆MHPG、焦虑-紧张和坐位收缩压的升高。这些观察结果表明,阿普唑仑的抗惊恐作用机制可能部分归因于苯二氮䓬敏感神经系统和去甲肾上腺素能神经系统之间的相互作用。