Thromboxane causes airway hyperresponsiveness following neurogenic
inflammation induced by cigarette smoke.
Matsumoto, Koichiro, Hisamichi Aizawa, Hiromasa Inoue, Mutsumi Shigyo,
Shohei Takata & Nobuyuki Hara.
Research Institute for Diseases of the Chest, Faculty of Medicine,
Kyushu University, 3-1-1 Maidashi, Higashiku, Fukuoka 812, Japan
APStracts 3:0366A, 1996.
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 (BALF).
FK224 (10 mg/kg i.v.), a tachykinin antagonist at NK1 and NK2
receptors, significantly inhibited these changes. The thromboxane
(TX) B2 concentration was increased in BALF after smoke exposure, and
was significantly inhibited by FK224. OKY-046 (10 mg/kg i.v.), 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.
Received 1 February 1996; accepted in final form 22 July 1996.
APS Manuscript Number A116-6.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 21 August 1996