对用花生四烯酸收缩的豚鼠气道反应的药理学调节。
Pharmacological modulation of responses of guinea-pig airways contracted with arachidonic acid.
作者信息
Burka J F
出版信息
Br J Pharmacol. 1985 Jun;85(2):421-5. doi: 10.1111/j.1476-5381.1985.tb08877.x.
Abstract
Arachidonic acid (AA) was used to induce contractions of guinea-pig tracheal and lung parenchymal preparations in the presence of indomethacin. Prior addition of FPL55712, nordihydroguaiaretic acid (NDGA), piriprost, benoxaprofen or nafazatrom, in order of potency, inhibited AA-induced contractions of trachea. Higher concentrations (2 - 3 fold) were necessary to inhibit contractions of parenchyma. FPL55712 and piriprost appeared to act as pharmacological antagonists of leukotrienes because they rapidly reduced the tone of the airways established by AA. Administration of exogenous AA to indomethacin-treated trachea appears to be a good model to examine leukotriene receptor antagonists and inhibitors of the lipoxygenase pathway.
摘要
在吲哚美辛存在的情况下，用花生四烯酸（AA）诱导豚鼠气管和肺实质制剂收缩。预先添加FPL55712、去甲二氢愈创木酸（NDGA）、吡嘧司特、苯恶洛芬或萘呋胺酯，按效力顺序抑制AA诱导的气管收缩。抑制实质收缩需要更高浓度（2至3倍）。FPL55712和吡嘧司特似乎作为白三烯的药理拮抗剂起作用，因为它们能迅速降低由AA建立的气道张力。向经吲哚美辛处理的气管施用外源性AA似乎是一种用于检测白三烯受体拮抗剂和脂氧合酶途径抑制剂的良好模型。
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