％0刊杂志文章％A Ishikawa，J％A ichinose，M％的Miura，M％A Kageyama，N％A Yamauchi，H％A Tomaki，M％A Sasaki，Y％A Shirato，k％的塞曲线，k％t参与内源性Tachykinins据报道，有限公司诱导的气道反应％D 1996％J欧洲呼吸期百分比P486-492％v 9％N 3％X白酮D4-（Ltd4）导致触艇从气道感官神经中释放。然而，内源性释放的Tachykinins在Ltd4介导的气道反应的功能意义尚未完全澄清。本研究的目的是调查是否有LTD4诱导的气道反应是部分原因是豚鼠中的Tachykinin释放。通过在阿托甘蓝型蓝色染料和普通丙氨酸（1mg.kg-1 i.v.）存在下，通过测量埃文斯蓝染料和平均肺抗性（R1）来评估气道等离子体渗出和支气管间。LTD4（5微克，1分1分钟）吸入引起的等离子体渗出和RL增加。辣椒素预处理动物耗尽感官神经肽显着抑制有限公司诱导的血浆在主要的支气管中渗出，但不在中央（CIPA）和外周血管通气管（PIPA）中。Pretreatment with specific tachykinin neurokinin-1 (NK1)-receptor antagonists, FK 888 (10 mg.kg-1 i.v.) and CP 96345 (4 mg.kg-1 i.v.), also significantly reduced LTD4-induced plasma exudation in the main bronchi, and in the main bronchi and cIPA, respectively. However, these antagonists did not significantly affect the LTD4-induced increase in RL. In contrast, neurokinin-2 (NK2)-receptor antagonist, SR 48968 (0.3 mg.kg-1 i.v.), significantly inhibited the bronchoconstriction after LTD4-inhalation. These results suggest that leukotriene D4-induced bronchoconstriction and plasma exudation in guinea-pigs are, in part, due to tachykinin release from airway sensory nerves. %U //www.qdcxjkg.com/content/erj/9/3/486.full.pdf