Misawa M, Sugiyama Y
Department of Pharmacology, School of Pharmacy, Hoshi University.
Arerugi. 1993 Feb;42(2):107-14.
We attempted to obtain a new airway hyperresponsiveness model using DNP-Ascaris extract (DNP-Asc)-induced rat allergic asthma. Male Wistar rats were actively sensitized with DNP-Asc, and challenged in a non-anesthetized state by inhalation of the antigen for 10 min in a chamber. One, 6 and 24 hr after DNP-Asc challenge, the responsiveness of the airway smooth muscles to inhaled acetylcholine (ACh) was determined using a modified Konzett-Rössler method under anesthesia. Twenty four hr after the challenge, a significant and marked airway hyperresponsiveness was seen. The increase in airway responsiveness was significantly inhibited by pretreatments with a leukotriene antagonist, ONO-1078, and a thromboxane synthetase inhibitor, ozagrel, and tended to be inhibited by a PAF antagonist, CV-3988. The hyperresponsiveness induced by DNP-Asc challenge was accompanied by airway inflammation determined by dye exudation. From the above results, it is indicated that a model of airway hyperresponsiveness was established in rats with allergic asthma, and that the chemical mediators involved in the response might be leukotrienes, thromboxane A2 and PAF.
我们试图使用二硝基苯基 - 蛔虫提取物（DNP - Asc）诱导的大鼠过敏性哮喘建立一种新的气道高反应性模型。雄性Wistar大鼠用DNP - Asc进行主动致敏，并在非麻醉状态下于密闭箱中吸入抗原10分钟进行激发。在DNP - Asc激发后1小时、6小时和24小时，在麻醉状态下使用改良的Konzett - Rössler方法测定气道平滑肌对吸入乙酰胆碱（ACh）的反应性。激发后24小时，观察到显著且明显的气道高反应性。用白三烯拮抗剂ONO - 1078和血栓素合成酶抑制剂奥扎格雷预处理可显著抑制气道反应性的增加，而血小板活化因子拮抗剂CV - 3988则有抑制气道反应性增加的趋势。DNP - Asc激发诱导的高反应性伴有通过染料渗出确定的气道炎症。根据上述结果表明，在过敏性哮喘大鼠中建立了气道高反应性模型，并且参与该反应的化学介质可能是白三烯、血栓素A2和血小板活化因子。
