JF欧洲呼吸杂志JO Eur Respir J FD欧洲呼吸学会SP 486 OP 492 DO 10.1183/09031936.96.09030486 VO 9 IS 3 A1 Ishikawa, J A1 Ichinose, M A1 Miura, M A1 Kageyama, N A1 Yamauchi, 188bet官网地址H A1 Tomaki, M A1 Sasaki, Y A1 Shirato，K YR 1996 UL //www.qdcxjkg.com/content/9/3/486.abstract AB白三烯D4-(LTD4)已被报道可引起气道感觉神经的速激肽释放。然而，内源性释放的速激肽在ltd4介导的气道反应中的功能意义尚未完全阐明。本研究的目的是调查ltd4诱导的气道反应是否部分归因于豚鼠的速激肽释放。通过测量埃文斯蓝染料的外渗和阿托品(1mg)存在时的平均肺阻力(RL)来评估气道血浆渗出和支气管收缩。Kg-1静脉注射)和心得安(1毫克)。Kg-1 i.v.)，分别。LTD4(5微克。mL-1 1 min)吸入引起血浆渗出和RL增加。辣椒素预处理可显著抑制ltd4诱导的主支气管血浆渗出，但对中心气道(cIPA)和外周肺内气道(pIPA)无抑制作用。预处理与特异性速激肽神经激肽-1 (NK1)受体拮抗剂，FK 888(10毫克。CP 96345 (4 mg。kg-1 i.v.)，也分别显著减少了ltd4在主支气管、主支气管和cIPA中诱导的血浆渗出。 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.