Dorsch W, Frey L
Naunyn Schmiedebergs Arch Pharmacol. 1981;317(4):351-6. doi: 10.1007/BF00501318.
Ovalbumin (OA) sensitized guinea pigs were repeatedly challenged with 1% OA in saline nebulized ultrasonically at the 0, 10, 20, 60 and 70th min. The intensity of bronchial obstruction was measured by body plethysmography. The first three challenges (0. 10, 20 min) caused strong asthmatic reactions in all animals, the last two (60, 70 min) only mild one in 10 out of 15 animals. The development of this "tachyphylaxis" was markedly reduced by pretreatment of the animals with cyclooxygenase inhibitors (indomethacin 10 mg/kg intraperitoneally resp, acetylsalicylic acid 10 mg/kg orally 2 h before tests). The effect of both inhibitors (i.e. inhibition of tachyphylaxis) was abolished by supplementing prostaglandin E2 as aerosol simultaneously to the allergen (100-200 ng per inhalation). The results suggest that allergen tachyphylaxis we have observed in vivo might be due to synthesis of cyclooxygenase products, e.g. prostaglandin E.
用卵清蛋白（OA）致敏豚鼠，在第0、10、20、60和70分钟时，用1%的OA生理盐水溶液经超声雾化反复激发。通过体容积描记法测量支气管阻塞的强度。前三次激发（0、10、20分钟）在所有动物中均引起强烈的哮喘反应，后两次（60、70分钟）在15只动物中的10只仅引起轻微反应。在用环氧化酶抑制剂预处理动物后（分别为腹腔注射吲哚美辛10mg/kg、在试验前2小时口服乙酰水杨酸10mg/kg），这种“快速减敏”的发展明显受到抑制。通过在激发变应原的同时以气雾剂形式补充前列腺素E2（每次吸入100 - 200ng），两种抑制剂的作用（即对快速减敏的抑制作用）均被消除。结果表明，我们在体内观察到的变应原快速减敏可能是由于环氧化酶产物的合成，例如前列腺素E。
