Winger G., Woods J.H.
Departments of Pharmacology Medical Science Research Building III, 1150 W. Medical Center Drive, University of Michigan, Ann Arbor, MI 48109-0632, USA.
Behav Pharmacol. 1996 Mar;7(2):155-159.
The mechanism by which buprenorphine reduces opioid self-administration in humans and animals is generally thought to be through its opioid agonist effects. Buprenorphine, given acutely i.v. to three rhesus monkeys 30min prior to a session in which a range of doses of either alfentanil or heroin was available, produced dose-related decreases in the potency of both opioid agonists. The effects of buprenorphine were generally surmounted by increasing the dose/injection of alfentanil or heroin available for self-administration, indicating that buprenorphine was acting as an opioid antagonist in this situation. These data suggest that at least part of the effectiveness of buprenorphine in reducing opioid administration by human opioid users may be via its opioid antagonist properties.
一般认为,丁丙诺啡降低人类和动物阿片类药物自我给药的机制是通过其阿片类激动剂作用。在恒河猴进行一系列剂量的阿芬太尼或海洛因自我给药实验前30分钟,静脉注射丁丙诺啡,结果显示两种阿片类激动剂的效力均出现剂量相关的降低。通过增加可供自我给药的阿芬太尼或海洛因的剂量/注射量,通常可以克服丁丙诺啡的作用,这表明在这种情况下丁丙诺啡起到了阿片类拮抗剂的作用。这些数据表明,丁丙诺啡在减少人类阿片类药物使用者阿片类药物使用方面的有效性,至少部分可能是通过其阿片类拮抗剂特性实现的。