De Nucci G, Astbury P, Read N, Salmon J A, Moncada S
Eur J Pharmacol. 1986 Jul 15;126(1-2):11-20. doi: 10.1016/0014-2999(86)90732-6.
The effect of dexamethasone on bradykinin-induced release of eicosanoids from isolated lungs of guinea-pigs exposed to pure oxygen (O2) is described. Pathological changes were induced in the lungs of guinea-pigs exposed to pure O2 for 72 and 96 h. Bradykinin-induced release of 6-oxo-PGF1 alpha and thromboxane B2 (TXB2) was increased in lungs from guinea-pigs exposed to 72 and 96 h of O2. Removal of PGI2 and PGE2 was not affected by the exposure to O2, but the removal of bradykinin was significantly reduced after 96 h of O2 exposure. Dexamethasone did not reduce bradykinin-induced release of eicosanoids from lungs of control animals, but it did inhibit the release from lungs of guinea-pigs exposed to O2. Dexamethasone had no effect on the metabolism of Bk by the inflamed lungs.
本文描述了地塞米松对缓激肽诱导的、来自暴露于纯氧（O₂）的豚鼠离体肺中类花生酸释放的影响。将豚鼠暴露于纯O₂ 72小时和96小时，可诱导肺部出现病理变化。在暴露于O₂ 72小时和96小时的豚鼠肺中，缓激肽诱导的6-氧代-PGF1α和血栓素B2（TXB2）释放增加。PGI2和PGE2的清除不受O₂暴露的影响，但在暴露于O₂ 96小时后，缓激肽的清除显著减少。地塞米松不会降低缓激肽诱导的对照动物肺中类花生酸的释放，但它确实抑制了暴露于O₂的豚鼠肺中的释放。地塞米松对炎症肺中Bk的代谢没有影响。
