Vinegar R, Truax J F, Selph J L, Welch R M, White H L, Ellis C H
Proc Soc Exp Biol Med. 1976 Mar;151(3):556-60. doi: 10.3181/00379727-151-39257.
Caffeine has been found to potentiate the acute anti-inflammatory activity of aspirin, indomethacin, and phenylbutazone, but not the activity of sodium salicylate or hydrocortisone, in the carrageenan pleurisy or hindlimb models of inflammation in the rat. The mobilization of inflammatory cells was not affected by aspirin in the presence or absence of caffeine. The mild analgesia produced by aspirin was confined to a hyperalgesic test in which this drug was able to reduce inflammation and concomitant hyperalgesia and thereby produce an "apparent" analgesic effect. This "apparent" analgesia produced by aspirin was potentiated by caffeine. The mechanism responsible for the potentiated anti-inflammatory and mild analgesic activity of aspirin remains unknown since caffeine did not alter the plasma salicylate levels or prostaglandin synthetase inhibition produced by aspirin.
在大鼠角叉菜胶性胸膜炎或后肢炎症模型中,已发现咖啡因可增强阿司匹林、吲哚美辛和保泰松的急性抗炎活性,但不能增强水杨酸钠或氢化可的松的活性。在有或没有咖啡因存在的情况下,阿司匹林均不影响炎症细胞的动员。阿司匹林产生的轻度镇痛作用仅限于一种痛觉过敏试验,在该试验中,这种药物能够减轻炎症和伴随的痛觉过敏,从而产生“明显的”镇痛效果。阿司匹林产生的这种“明显的”镇痛作用可被咖啡因增强。由于咖啡因不会改变阿司匹林产生的血浆水杨酸盐水平或对前列腺素合成酶的抑制作用,因此阿司匹林抗炎和轻度镇痛活性增强的机制仍然未知。