Post R M, Rubinow D R, Uhde T W, Ballenger J C, Lake C R, Linnoila M, Jimerson D C, Reus V
Psychopharmacology (Berl). 1985;87(1):59-63. doi: 10.1007/BF00431779.
Noradrenergic mechanisms have been postulated to account for the anticonvulsant and psychotropic effects of carbamazepine. In order to assess this possibility in man, cerebrospinal fluid (CSF) was obtained from affectively ill patients before and during treatment with carbamazepine (average duration 29 days) at doses averaging 860 mg/day, achieving blood levels of 8.86 micrograms/ml. Neither plasma nor CSF norepinephrine (NE) nor CSF 3-methoxy-4-hydroxy-phenylglycol (MHPG) was significantly altered by carbamazepine. Baseline medication-free values in 21 depressed patients were not predictive of the degree of subsequent clinical antidepressant response. CSF NE decreased in four manic patients treated with carbamazepine. The many effects of carbamazepine on noradrenergic mechanisms in animals are discussed in relationship to these first studies of carbamazepine in man.
去甲肾上腺素能机制被认为与卡马西平的抗惊厥和精神otropic作用有关。为了在人体中评估这种可能性,在平均剂量为860毫克/天、血药浓度达到8.86微克/毫升的卡马西平治疗前和治疗期间(平均持续29天),从情感障碍患者中获取脑脊液(CSF)。卡马西平对血浆或脑脊液去甲肾上腺素(NE)以及脑脊液3-甲氧基-4-羟基苯乙二醇(MHPG)均无显著影响。21例抑郁症患者的基线无用药值并不能预测随后临床抗抑郁反应的程度。在接受卡马西平治疗的4例躁狂患者中,脑脊液NE降低。结合这些关于卡马西平在人体中的初步研究,讨论了卡马西平在动物体内对去甲肾上腺素能机制的多种作用。