Weichman B M, Berkenkopf J W, Cullinan C A, Sturm R J
Department of Pharmacology, Ayerst Laboratories Research, Princeton, NJ 08543-9990.
Agents Actions. 1987 Aug;21(3-4):351-4. doi: 10.1007/BF01966513.
Immunoreactive leukotriene B4 (iLTB4), detected in the pleural cavity following induction of a reverse passive Arthus reaction (RPAR), was inhibited by the mixed lipoxygenase-cyclooxygenase inhibitors, phenidone and BW 755C, but not by cyclooxygenase inhibitors or by chlorpheniramine or methysergide. Both iLTB4 production and the subsequent pleural inflammation were dependent upon the dose of BSA antigen employed to elicit the RPAR pleurisy. However, inasmuch as BW 755C and phenidone were not distinguished from the cyclooxygenase inhibitors in their effects on fluid accumulation and cellular infiltration in RPAR pleurisy, it is doubtful that LTB4 plays a functional role in this inflammation model.
在诱导反向被动阿瑟斯反应（RPAR）后，在胸腔中检测到的免疫反应性白三烯B4（iLTB4）受到脂氧合酶 - 环氧化酶混合抑制剂非那吡啶和BW 755C的抑制，但不受环氧化酶抑制剂、氯苯那敏或甲基麦角新碱的抑制。iLTB4的产生以及随后的胸膜炎均取决于用于引发RPAR胸膜炎的牛血清白蛋白（BSA）抗原的剂量。然而，由于BW 755C和非那吡啶在对RPAR胸膜炎中液体蓄积和细胞浸润的影响方面与环氧化酶抑制剂没有区别，因此怀疑LTB4在该炎症模型中是否发挥功能作用。
