Sindrup S H, Arendt-Nielsen L, Brøsen K, Bjerring P, Angelo H R, Eriksen B, Gram L F
Department of Clinical Pharmacology, Odense University, Aalborg University.
Eur J Clin Pharmacol. 1992;42(6):587-91. doi: 10.1007/BF00265920.
We have studied the hypoalgesic effect of codeine (100 mg) after blocking the hepatic O-demethylation of codeine to morphine via the sparteine oxygenase (CYP2D6) by quinidine (200 mg). The study was performed in 16 extensive metabolizers of sparteine, using a double-blind, randomized, four-way, cross-over design. The treatments given at 3 h intervals during the four sessions were placebo/placebo, quinidine/placebo, placebo/codeine, and quinidine/codeine. We measured pinprick pain and pain tolerance thresholds to high energy argon laser stimuli before and 1, 2, and 3 h after codeine or placebo. After codeine and placebo, the peak plasma concentration of morphine was 6-62 (median 18) nmol.l-1. When quinidine pre-treatment was given, no morphine could be detected (less than 4 nmol.l-1) after codeine. The pin-prick pain thresholds were significantly increased after placebo/codeine, but not after quinidine/codeine compared with placebo/placebo. Both placebo/codeine and quinidine/codeine increased pain tolerance thresholds significantly. Quinidine/codeine and quinidine/placebo did not differ significantly for either pin-prick or tolerance pain thresholds. These results are compatible with local CYP2D6 mediated formation of morphine in the brain, not being blocked by quinidine. Alternatively, a hypoalgesic effect of quinidine might have confounded the results.
我们研究了通过奎尼丁(200mg)阻断可待因经司巴丁氧化酶(CYP2D6)向吗啡的肝脏O-去甲基化作用后,可待因(100mg)的镇痛作用减弱效应。该研究在16名司巴丁广泛代谢者中进行,采用双盲、随机、四组交叉设计。在四个疗程中,每隔3小时给予的治疗分别为安慰剂/安慰剂、奎尼丁/安慰剂、安慰剂/可待因和奎尼丁/可待因。我们在给予可待因或安慰剂之前以及之后1、2和3小时测量了针刺疼痛和对高能氩激光刺激的疼痛耐受阈值。给予可待因和安慰剂后,吗啡的血浆峰值浓度为6 - 62(中位数18)nmol·l-1。给予奎尼丁预处理后,服用可待因后未检测到吗啡(低于4nmol·l-1)。与安慰剂/安慰剂相比,安慰剂/可待因后针刺疼痛阈值显著升高,但奎尼丁/可待因后未升高。安慰剂/可待因和奎尼丁/可待因均显著提高了疼痛耐受阈值。奎尼丁/可待因和奎尼丁/安慰剂在针刺或耐受疼痛阈值方面无显著差异。这些结果与大脑中局部CYP2D6介导的吗啡形成未被奎尼丁阻断一致。或者,奎尼丁的镇痛作用可能混淆了结果。