TY -的T1的参与速激肽NK1 P-induced微血管渗漏和NK2受体物质过敏,在因为豚鼠气道高反应JF -欧洲呼吸杂志》乔和J SP - 1445 LP - 1450欧元六世- 9 - 7盟Boichot E盟——Biyah K AU -日尔曼,N盟——Emonds-Alt X盟——Lagente V盟——Advenier C Y1 - 1996/07/01 UR - //www.qdcxjkg.com/content/9/7/1445.abstract N2 -速激肽,如P物质、可能参与了气道高反应性(AHR)和气道炎症的发生。然而，目前尚不清楚是哪一种心动过速素受体介导了这些生物活性。研究了两种抗速激肽神经激肽-1 (NK1)和速激肽-2 (NK2)受体SR 140333和SR 48968对磷酰胺预处理豚鼠P物质诱导的气道高反应性和组胺诱导的微血管渗漏增加的增强作用。用磷酰胺预处理豚鼠(0.1 mM气雾剂15分钟)，15分钟后单独暴露于生理盐水或含SP的生理盐水(0.1 mg)中。mL-1 30分钟)。24小时后，动物被麻醉，准备记录乙酰胆碱的肺充气压力(PIP)，或调查组胺的微血管渗漏。单剂量SR 48968 (1 mg)预处理豚鼠。SP暴露前30分钟，kg-1 (i.p.)显著阻止AHR的发生，而SR 140333 (1 mg)。kg-1 (i.p.)没有。在第二组实验中，磷酰胺预处理豚鼠暴露于SP后，组胺诱导的气道微血管渗漏明显增强。当用SR 140333预处理豚鼠时，观察到对组胺增加的微血管渗漏的抑制作用。 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. ER -