Effect of caffeine coadministration and of nitric oxide synthesis inhibition on the antinociceptive action of ketorolac.
Effect of caffeine coadministration and of nitric oxide synthesis inhibition on the antinociceptive action of ketorolac.
复制标题
咖啡因共同给药和一氧化氮合成抑制对酮咯酸抗伤害作用的影响。
DOI：
10.1016/0014-2999(96)00320-2
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发表时间：
1996
影响因子：
5
通讯作者：
V. Granados
中科院分区：
文献类型：
--
作者：
F. López;G. Castañeda;F. Flores;V. Granados
使用大鼠疼痛诱发的功能损伤模型评估咖啡因和一氧化氮合成抑制对酮咯酸抗伤害作用的影响。通过关节内注射尿酸诱导伤害感受。酮咯酸（而非咖啡因）产生镇痛作用，该作用会被一氧化氮合成抑制剂 NG-硝基-L-精氨酸甲酯 (L-NAME) 减弱。咖啡因的共同给药增强了酮咯酸的作用。 l-NAME 诱导这种增强作用的剂量依赖性降低。结果表明，L-精氨酸-一氧化氮-环 GMP 途径参与咖啡因增强酮咯酸诱导的镇痛作用。
The effects of caffeine and nitric oxide synthesis inhibition on the antinociceptive action of ketorolac were assessed using the pain-induced functional impairment model in the rat. Nociception was induced by the intra-articular injection of uric acid. Ketorolac, but not caffeine, produced an antinociceptive effect which was reduced by NG-nitro-l-arginine methyl ester (l-NAME), an inhibitor of nitric oxide synthesis. Caffeine coadministration potentiated the ketorolac effect. l-NAME induced a dose-dependent reduction of this potentiation. The results suggest the participation of the l-arginine-nitric oxide-cyclic GMP pathway in the caffeine potentiation of ketorolac-induced antinociception.