Moises H W, Beckmann H
J Neural Transm. 1981;50(2-4):185-92. doi: 10.1007/BF01249140.
The (+)- and (-)-isomers of the monoamine oxidase inhibitor (MAO-I) tranylcypromine (TCP) were administered separately in a double-blind controlled study to 20 depressed patients. The Hamilton Depression Rating Scale, the AMP-system and the Bf-s self-rating questionnaire were used for documentation of psychopathological state and autonomic side effects. Overall there was a statistically significant decrease in the Hamilton depression scores (p less than 0.01 for the (+)-isomer, but not for the (-)-isomer group, whereas self-rating scores did not show a significant decrease in either group. Autonomic side effects were more pronounced (p less than 0.05) in the (+)-isomer group. As platelet MAO was significantly stronger (p less than 0.001) inhibited in the (+)-TCP group as compared with the (-)-TCP group, it is suggested that MAO inhibition rather than uptake blockade is the biochemical mechanism responsible for both the antidepressant activity and the autonomic side effects due to TCP medication.
在一项双盲对照研究中,将单胺氧化酶抑制剂(MAO-I)反苯环丙胺(TCP)的(+)-和(-)-异构体分别给予20名抑郁症患者。使用汉密尔顿抑郁量表、AMP系统和Bf-s自评问卷来记录心理病理状态和自主神经副作用。总体而言,汉密尔顿抑郁评分有统计学显著下降((+)-异构体组p<0.01,但(-)-异构体组无下降),而两组的自评评分均未显示出显著下降。(+)-异构体组的自主神经副作用更明显(p<0.05)。与(-)-TCP组相比,(+)-TCP组血小板MAO受到的抑制显著更强(p<0.001),这表明MAO抑制而非摄取阻断是TCP药物治疗导致抗抑郁活性和自主神经副作用的生化机制。