Thromboxane causes airway hyperresponsiveness after cigarette smoke-induced neurogenic inflammation

Koichiro Matsumoto, Hisamichi Aizawa, Hiromasa Inoue, Mutsumi Shigyo, Shohei Takata, Nobuyuki Hara

研究成果: ジャーナルへの寄稿学術誌査読

20 被引用数 (Scopus)


We investigated the role of neurogenic inflammation and the subsequent mechanisms in cigarette smoke-induced airway hyperresponsiveness in guinea pigs. Exposure to cigarette smoke was carried out at tidal volume for 3 min. Airway responsiveness to histamine was determined before and after smoke exposure followed by bronchoalveolar lavage (BAL). Plasma extravasation was evaluated by measuring the extravasation of Evans blue dye in the airway. Cigarette smoke produced significant airway hyperresponsiveness and plasma extravasation, with an influx of neutrophils in BAL fluid. FK-224 (10 mg/kg iv), a tachykinin antagonist at NK1 and NK2 receptors, significantly inhibited these changes. The thromboxane (Tx) B2 concentration was increased in BAL fluid after smoke exposure and was significantly inhibited by FK-224. OKY-046 (10 mg/kg iv), a Tx synthase inhibitor, significantly inhibited airway hyperresponsiveness but had no effect on neutrophil influx or plasma extravasation. The results suggest that neurogenic inflammation and the subsequent generation of Tx in the airway are important in the development of the airway hyperresponsiveness induced by cigarette smoke.

ジャーナルJournal of Applied Physiology
出版ステータス出版済み - 12月 1996

!!!All Science Journal Classification (ASJC) codes

  • 生理学
  • 生理学(医学)


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