Bergren D R, Kincaid R J
Prostaglandins Leukot Med. 1984 Nov;16(2):163-71. doi: 10.1016/0262-1746(84)90068-4.
The effects of leukotriene C4 (LTC4), prostaglandin F2 alpha (PGF2 alpha), histamine, and bradykinin upon intratracheal pressure and nerve activity from rapidly-adapting receptors (RARs) before and after the nonsteroidal anti-inflammatory drugs salicylic acid (SA) and aspirin (ASA, acetylsalicylic acid) have been studied in guinea pigs. All mediators increased tracheal pressure and nerve activity in a time-dependent manner. The peak in nerve activity always preceded the peak in tracheal pressure. Neither SA or ASA blocked the effects of histamine or PGF2 alpha upon tracheal pressure or nerve activity. ASA and even SA blocked the effects of bradykinin on both parameters. While SA had no effect on LTC4, ASA blocked the effects of LTC4 upon both tracheal pressure and nerve activity. These results suggest that both LTC4 and bradykinin may act through mediators derived from arachidonic acid not only in increasing tracheal pressures but also to increase RAR nerve activity.
在豚鼠身上研究了白三烯C4（LTC4）、前列腺素F2α（PGF2α）、组胺和缓激肽对气管内压力以及非甾体抗炎药水杨酸（SA）和阿司匹林（ASA，乙酰水杨酸）作用前后快速适应受体（RAR）神经活动的影响。所有介质均以时间依赖性方式增加气管压力和神经活动。神经活动的峰值总是先于气管压力的峰值出现。SA和ASA均未阻断组胺或PGF2α对气管压力或神经活动的影响。ASA甚至SA阻断了缓激肽对这两个参数的影响。虽然SA对LTC4没有影响，但ASA阻断了LTC4对气管压力和神经活动的影响。这些结果表明，LTC4和缓激肽可能不仅通过源自花生四烯酸的介质来增加气管压力，还能增加RAR神经活动。
