Walker J R, Woodhouse S A
Lilly Research Centre Ltd, Eli Lilly & Co., Surrey, UK.
Agents Actions. 1989 Jan;26(1-2):99-102. doi: 10.1007/BF02126572.
The 5-lipoxygenase inhibitors, AA861 and phenidone, have been shown to inhibit the formation and release of leukotrienes C4, D4 and B4 from isolated perfused sensitised guinea pigs lungs when challenged through either the pulmonary system or the airways. The same drugs inhibit the thoracic neutrophil, but not platelet, accumulation observed following i.v. antigen challenge of sensitised guinea pigs. Indomethacin, a cyclooxygenase inhibitor, at doses which inhibited an arachidonic acid-induced thoracic platelet accumulation, had no effect on the platelet response following antigen challenge. Indomethacin did affect, however, the neutrophil response to antigen challenge presumably through mechanisms unrelated to cyclooxygenase inhibition. These observations suggest a role for lipoxygenase products, possibly LTB4, but not cyclooxygenase products in the neutrophil response to i.v. antigen challenge.
5-脂氧合酶抑制剂AA861和非那宗已被证明，当通过肺系统或气道进行激发时，它们可抑制致敏豚鼠离体灌注肺中白三烯C4、D4和B4的形成与释放。同样的药物可抑制致敏豚鼠静脉注射抗原激发后观察到的胸腔中性粒细胞聚集，但对血小板聚集无抑制作用。环氧化酶抑制剂吲哚美辛在抑制花生四烯酸诱导的胸腔血小板聚集的剂量下，对抗原激发后的血小板反应没有影响。然而，吲哚美辛确实影响了中性粒细胞对抗原激发的反应，推测其作用机制与环氧化酶抑制无关。这些观察结果表明，脂氧合酶产物，可能是白三烯B4，而非环氧化酶产物在中性粒细胞对静脉注射抗原激发的反应中发挥作用。
