Maddock R J, Carter C S, Magliozzi J R, Gietzen D W
Department of Psychiatry, University of California, School of Medicine, Davis.
Am J Psychiatry. 1993 Aug;150(8):1219-25. doi: 10.1176/ajp.150.8.1219.
This study was designed to clarify the nature of the reduced function of the peripheral beta adrenoceptor system observed in panic disorder with agoraphobia. The authors hypothesized that this phenomenon reflected a regulatory and adaptive process.
Lymphocyte beta adrenoreceptor density and affinity, basal lymphocyte cAMP level, and isoproterenol-stimulated cAMP generation were measured in 27 untreated outpatients with panic disorder with agoraphobia and 24 healthy comparison subjects. Lymphocyte beta receptor attributes were again assessed in patients after 4 weeks of double-blind treatment with adinazolam (slow-release form) or placebo. Panic frequency, agoraphobic symptoms, overall anxiety, and improvement with treatment were assessed with standard rating instruments.
Multivariate statistics revealed significantly lower beta receptor density and isoproterenol-stimulated cAMP generation in patients than in comparison subjects. beta receptor density tended to normalize after adinazolam but not after placebo. Pretreatment beta receptor density was lower in treatment responders than nonresponders. Patients with mild agoraphobia had lower cAMP responsivity than patients with moderate or severe agoraphobia.
Decreased function of lymphocyte beta receptors in panic disorder with agoraphobia is expressed as both decreased density and decreased cAMP responsivity. This pattern of changes, and the tendency for receptor density to normalize with treatment, is consistent with an active, regulatory process rather than a structural deficit in the beta receptor system. Preliminary clinical findings suggest that these changes may reflect adaptive processes associated with a favorable clinical course in panic disorder with agoraphobia.
本研究旨在阐明在伴有广场恐怖症的惊恐障碍中观察到的外周β肾上腺素能受体系统功能减退的本质。作者推测这一现象反映了一种调节和适应过程。
对27名未经治疗的伴有广场恐怖症的惊恐障碍门诊患者和24名健康对照者测量淋巴细胞β肾上腺素能受体密度和亲和力、基础淋巴细胞环磷酸腺苷（cAMP）水平以及异丙肾上腺素刺激后的cAMP生成。在用阿地唑仑（缓释剂型）或安慰剂进行4周双盲治疗后，再次评估患者的淋巴细胞β受体特性。用标准评定工具评估惊恐发作频率、广场恐怖症状、总体焦虑程度以及治疗后的改善情况。
多变量统计显示，患者的β受体密度和异丙肾上腺素刺激后的cAMP生成显著低于对照者。阿地唑仑治疗后β受体密度趋于正常化，而安慰剂治疗后则不然。治疗反应者的治疗前β受体密度低于无反应者。轻度广场恐怖症患者的cAMP反应性低于中度或重度广场恐怖症患者。
伴有广场恐怖症的惊恐障碍中淋巴细胞β受体功能减退表现为密度降低和cAMP反应性降低。这种变化模式以及受体密度随治疗趋于正常化的趋势，与一个活跃的调节过程一致，而不是β受体系统的结构缺陷。初步临床研究结果表明，这些变化可能反映了与伴有广场恐怖症的惊恐障碍良好临床病程相关的适应过程。
