RT期刊文章SR电子T1旋转金蛋白NK1和NK2受体参与物质P诱导的微血管泄漏超敏性和气道高反应性在豚鼠JF欧洲呼吸道188bet官网地址，e a1 biyah，k a1 germain，n a1 emonds-alt，x a1 lagente，v a1 advenier，c yr 1996 ul //www.qdcxjkg.com/content.com/content/9/9/7/1445.1445.Abstract作为P，可能参与气道高反应性（AHR）和气道炎症的发展。但是，尚不清楚哪种速素受体介导这些生物学活性。分别研究了两种旋转神经蛋白神经蛋白1（NK1）和吉跃蛋白神经蛋白-2（NK2）受体SR 140333和SR 48968的拮抗剂的作用。在磷光灯下豚鼠中，微血管泄漏的增加。将豚鼠用磷光灯（0.1 mM气雾剂15分钟）预处理，并在15分钟后暴露于单独的盐水溶液或含有SP（0.1 mg.ml-1 30分钟）的盐水溶液中。二十四小时后，将动物麻醉并准备好记录肺通胀压力（PIP）到乙酰胆碱或研究微血管渗漏到组胺中的研究。在SP暴露前30分钟以单剂量的SR 48968（1 mg.kg-1，i.p.）对豚鼠进行预处理，显着阻止了AHR的发展，而SR 140333（1 mg.kg.kg-1，i.p.）确实做到了不是。在第二组实验中，暴露于SP的磷光灯磷脂预处理的豚鼠显着增强了组胺诱导的肺气道中微血管泄漏的增加。 When the guinea-pigs were pretreated with SR 140333, an inhibition of the increased microvascular leakage to histamine was observed. In contrast, no significant inhibitory activity was noted when the guinea-pigs were pretreated with SR 48968. The present data demonstrate the importance of tachykinin NK2 receptor stimulation in the development of airway hyperresponsiveness and that of tachykinin NK1 receptor stimulation in microvascular leakage hypersensitivity in phosphoramidon-pretreated and substance P-exposed guinea-pigs. The results also suggest a dissociation between the presence of microvascular leakage and the occurrence of airway hyperresponsiveness.