Adcock J J, Garland L G, Moncada S, Salmon J A
Prostaglandins. 1978 Aug;16(2):179-87. doi: 10.1016/0090-6980(78)90020-5.
Indomethacin augmented the release of histamine and SRS-A but abolished synthesis of TxB2. Compound CLI that inhibited both cyclo-oxygenase and lipoxygenase pathways of arachidonic acid metabolism did not augment release of anaphylactic mediators. 13-HPLA enhanced mediator release from lungs in which arachidonic acid metabolism was blocked by compount CLI. Thus, it is concluded that 13-HPLA enhances mediator release not by altering the balance of arachidonic acid metabolites, e.g. by inhibiting synthesis of prostacyclin, but by a direct effect on lung mast cells. A corollary to this conclusion is that the fatty acid hydroperoxide (HPETE) formed by lipoxygenase from arachidonic acid may also augment the release of anaphylactic mediators. Thus, the enhancement of mediator release by indomethacin may be attributed to increased synthesis of HPETE following inhibition of cyclo-oxygenase.
吲哚美辛增加了组胺和慢反应物质A的释放，但抑制了血栓素B2的合成。抑制花生四烯酸代谢的环氧化酶和脂氧化酶途径的化合物CLI并没有增加过敏介质的释放。13-氢过氧-5,8,11,14-二十碳四烯酸（13-HPLA）增强了化合物CLI阻断花生四烯酸代谢的肺组织中介质的释放。因此，可以得出结论，13-HPLA增强介质释放不是通过改变花生四烯酸代谢产物的平衡，例如通过抑制前列环素的合成，而是通过对肺肥大细胞的直接作用。这个结论的一个推论是，脂氧化酶由花生四烯酸形成的脂肪酸氢过氧化物（HPETE）也可能增加过敏介质的释放。因此，吲哚美辛对介质释放的增强作用可能归因于环氧化酶抑制后HPETE合成的增加。
