Matsumoto K, Aizawa H, Inoue H, Takata S, Shigyo M, Hara N
Research Institute for Diseases of the Chest, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Eur Respir J. 1996 Dec;9(12):2468-73. doi: 10.1183/09031936.96.09122468.
Acute exposure to cigarette smoke provokes bronchoconstriction and increases the concentration of thromboxane (Tx) A2 in bronchoalveolar lavage (BAL) fluid. The purpose of this study was to investigate the role of TxA2 and cholinergic mechanisms in the airway response induced by exposure to cigarette smoke in guinea-pigs. Anaesthetized animals were exposed to 200 puffs of smoke for 10 min. The amount of Evans blue dye extravasated into the bronchial tissue was then measured BAL was performed to determine cell counts and the concentration of TxB2, a stable metabolite of TxA2. The effects of pretreatment with a Tx synthase inhibitor, OKY-046 (10 mg.kg-1), and/or atropine (1 mg.kg-1) were evaluated. Exposure to cigarette smoke caused significant bronchoconstriction (284 +/- 33% of baseline pulmonary resistance (RL)) and plasma extravasation (30.0 +/- 3.8 vs 16.8 +/- 2.6 ng.mg-1 of sham control; main bronchi). OKY-046 or atropine significantly inhibited the bronchoconstriction to a similar extent, without affecting the plasma extravasation. Combined use of these compounds had no additive effect. The cigarette smoke caused significant increase in TxB2 (48 +/- 10 vs 14 +/- 1 pg.mL-1 of sham control) in BAL fluid, which was abolished by OKY-046 but not by atropine. The cellularity in BAL fluid was not different among groups. These results suggest that the bronchoconstriction induced by cigarette smoke is partially mediated by thromboxane A2, which is dependent on a cholinergic pathway.
急性暴露于香烟烟雾会引发支气管收缩，并增加支气管肺泡灌洗（BAL）液中血栓素（Tx）A2的浓度。本研究的目的是探讨TxA2和胆碱能机制在豚鼠暴露于香烟烟雾所诱导的气道反应中的作用。将麻醉的动物暴露于200口烟雾中10分钟。然后测量渗入支气管组织的伊文思蓝染料量，进行BAL以确定细胞计数和TxA2的稳定代谢产物TxB2的浓度。评估用Tx合酶抑制剂OKY - 046（10mg·kg-1）和/或阿托品（1mg·kg-1）预处理的效果。暴露于香烟烟雾会导致显著的支气管收缩（基线肺阻力（RL）的284±33%）和血浆外渗（主支气管处为30.0±3.8 vs假手术对照组的16.8±2.6 ng·mg-1）。OKY - 046或阿托品在相似程度上显著抑制了支气管收缩，而不影响血浆外渗。联合使用这些化合物没有相加作用。香烟烟雾使BAL液中TxB2显著增加（48±10 vs假手术对照组的14±1 pg·mL-1），这被OKY - 046消除，但未被阿托品消除。各组BAL液中的细胞数没有差异。这些结果表明，香烟烟雾诱导的支气管收缩部分由血栓素A2介导，其依赖于胆碱能途径。
