Lôo H, Benkelfat C, Poirier M F, Gay C, Askienazy S, Dennis T, Scatton B
Neuropsychobiology. 1986;15(2):68-72. doi: 10.1159/000118244.
Escape from dexamethasone-induced suppression of plasma cortisol is an abnormality found in about half of patients with major depression. It has been hypothesized that this hyperactivity of the hypothalamo-pituitary-adrenal axis might be related to a central noradrenergic hypofunction. The present study was designed to test this hypothesis by measuring plasma 3,4-dihydroxyphenylethyleneglycol (DOPEG) levels (free and conjugated forms), an index of central noradrenergic activity, and by simultaneously carrying out a dexamethasone suppression test. Forty-five patients with a diagnosis of major depression (according to the DSM-III) were investigated. Plasma DOPEG levels (measured at 8 a.m.) were found to be similar in dexamethasone suppressor and nonsuppressor depressed patients. These results do not support the hypothesis that central noradrenergic hypoactivity underlies nonsuppression of dexamethasone in major depression.
从地塞米松诱导的血浆皮质醇抑制中逃逸是约半数重度抑郁症患者中发现的一种异常情况。据推测，下丘脑-垂体-肾上腺轴的这种功能亢进可能与中枢去甲肾上腺素能功能减退有关。本研究旨在通过测量血浆3,4-二羟基苯乙二醇（DOPEG）水平（游离和结合形式）（中枢去甲肾上腺素能活性指标）并同时进行地塞米松抑制试验来检验这一假设。对45例诊断为重度抑郁症（根据《精神疾病诊断与统计手册》第三版）的患者进行了调查。发现地塞米松抑制者和非抑制者的抑郁症患者上午8点测得的血浆DOPEG水平相似。这些结果不支持以下假设，即中枢去甲肾上腺素能功能减退是重度抑郁症患者地塞米松抑制试验不被抑制的基础。
