Ahlijanian M K, Takemori A E
Eur J Pharmacol. 1985 Jun 7;112(2):171-9. doi: 10.1016/0014-2999(85)90493-5.
(-)-N6-(R-phenylisopropyl)-adenosine (PIA) was shown to possess analgesic activity in both the tail flick and acetic acid writhing assays. The analgesic actions of PIA were antagonized by caffeine in a dose-dependent manner. An apparent pA2 analysis in vivo suggested that the antagonism by caffeine was not competitive. Subanalgesic doses of PIA potentiated morphine-induced analgesia, tolerance and dependence. Caffeine antagonized these effects of morphine. PIA attenuated while caffeine exacerbated opiate withdrawal. While a low dose of caffeine antagonized PIA effects on withdrawal, a low dose of PIA did not antagonize the effects of caffeine. These results indicate that PIA can facilitate, and caffeine can antagonize the actions of morphine and that caffeine may be exerting some of its actions independent of adenosine receptor antagonism.
（-）-N6-（R-苯异丙基）-腺苷（PIA）在甩尾试验和醋酸扭体试验中均显示出镇痛活性。PIA的镇痛作用被咖啡因以剂量依赖性方式拮抗。体内的表观pA2分析表明，咖啡因的拮抗作用并非竞争性的。亚镇痛剂量的PIA增强了吗啡诱导的镇痛、耐受性和依赖性。咖啡因拮抗了吗啡的这些作用。PIA减轻了阿片类药物戒断反应，而咖啡因则加剧了这种反应。虽然低剂量的咖啡因拮抗了PIA对戒断反应的影响，但低剂量的PIA并未拮抗咖啡因的作用。这些结果表明，PIA可以促进吗啡的作用，而咖啡因可以拮抗吗啡的作用，并且咖啡因可能在不依赖腺苷受体拮抗作用的情况下发挥其某些作用。
