Liebowitz M R, Karoum F, Quitkin F M, Davies S O, Schwartz D, Levitt M, Linnoila M
Biol Psychiatry. 1985 May;20(5):558-65. doi: 10.1016/0006-3223(85)90027-7.
To examine the biochemical effects of 10-30 mg/day L-deprenyl, measurement of 24-hr urinary output of phenylethylamine (PEA), 3-methoxy 4-hydroxy phenylethyleneglycol (MHPG), and L-deprenyl's amphetamine metabolites were carried out before and during the treatment of atypical depressives. Platelet monoamine oxidase (MAO) activity was also assessed. With L-deprenyl 10-30 mg/day, the expected MAO B inhibition occurred, as indicated by significant increase in urinary PEA excretion and virtual disappearance of platelet MAO activity. Twenty-five to 33% of the daily dose of L-deprenyl was recovered as urinary methamphetamine or amphetamine. Excretion of MHPG was significantly decreased with L-deprenyl 10-20 mg/day. Overall, the results suggest that L-deprenyl's antidepressant effects are mediated by some mechanism other than, or in addition to, MAO B inhibition.
为研究每天10 - 30毫克L - 司来吉兰的生化效应,在非典型抑郁症患者治疗前及治疗期间,对苯乙胺(PEA)、3 - 甲氧基4 - 羟基苯乙二醇(MHPG)的24小时尿排泄量以及司来吉兰的苯丙胺代谢产物进行了测量。还评估了血小板单胺氧化酶(MAO)活性。服用每天10 - 30毫克的司来吉兰后,出现了预期的MAO B抑制作用,尿PEA排泄显著增加以及血小板MAO活性几乎消失表明了这一点。司来吉兰每日剂量的25%至33%以尿甲基苯丙胺或苯丙胺的形式回收。服用每天10 - 20毫克司来吉兰后,MHPG的排泄显著减少。总体而言,结果表明司来吉兰的抗抑郁作用是由MAO B抑制以外的某种机制介导的,或者是在此基础上还有其他机制。