Burka J F
Prostaglandins. 1985 Apr;29(4):529-35. doi: 10.1016/0090-6980(85)90077-2.
Ovalbumin (OA) and arachidonic acid (AA) were used to induce contractions of sensitized guinea-pig tracheal and lung preparations in the presence and absence of indomethacin. Leukotriene (LT)C4-like material released from these tissues was extracted from the bathing fluid and measured by radioimmunoassay. Challenge with either OA or AA induced release of LTC4-like material from both parenchyma and trachea, AA inducing a greater release than OA although OA induced greater contractions. This suggested that OA-induced the synthesis of other bronchoconstrictor compounds than LTC4. Although indomethacin enhanced OA- and AA-induced contractions of trachea, there was no enhancement of the release of LTC4-like material, suggesting enhancement by indomethacin was a result of the inhibition of the synthesis of prostaglandin E2 and not diversion of AA into the lipoxygenase pathway. Indomethacin had no effect on OA-induced contractions of parenchyma, but attenuated those induced by AA. Indomethacin had no modulatory effect on the release of LTC4-like material in the parenchyma. The results demonstrate that indomethacin does not result in increased synthesis of LTs in the airways.
在有和没有吲哚美辛的情况下，使用卵清蛋白（OA）和花生四烯酸（AA）诱导致敏豚鼠气管和肺组织的收缩。从这些组织中释放的白三烯（LT）C4样物质从浴液中提取，并用放射免疫分析法进行测量。用OA或AA刺激均可诱导实质组织和气管释放LTC4样物质，尽管OA诱导的收缩更强，但AA诱导的释放量比OA更大。这表明OA诱导合成的支气管收缩化合物不是LTC4。虽然吲哚美辛增强了OA和AA诱导的气管收缩，但并没有增强LTC4样物质的释放，这表明吲哚美辛的增强作用是由于抑制了前列腺素E2的合成，而不是AA转向脂氧合酶途径。吲哚美辛对OA诱导的实质组织收缩没有影响，但减弱了AA诱导的收缩。吲哚美辛对实质组织中LTC4样物质的释放没有调节作用。结果表明，吲哚美辛不会导致气道中白三烯合成增加。
