Thromboxane causes airway hyperresponsiveness after cigarette smoke-induced neurogenic inflammation

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

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)2358-2364
Number of pages7
JournalJournal of Applied Physiology
Volume81
Issue number6
DOIs
Publication statusPublished - Dec 1996

Fingerprint

Neurogenic Inflammation
Thromboxanes
Smoke
Tobacco Products
FK 224
Bronchoalveolar Lavage Fluid
Neutrophils
Tachykinins
Thromboxane B2
Evans Blue
Tidal Volume
Bronchoalveolar Lavage
Histamine
Guinea Pigs
Coloring Agents

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

Thromboxane causes airway hyperresponsiveness after cigarette smoke-induced neurogenic inflammation. / Matsumoto, Koichiro; Aizawa, Hisamichi; Inoue, Hiromasa; Shigyo, Mutsumi; Takata, Shohei; Hara, Nobuyuki.

In: Journal of Applied Physiology, Vol. 81, No. 6, 12.1996, p. 2358-2364.

Research output: Contribution to journalArticle

Matsumoto, Koichiro ; Aizawa, Hisamichi ; Inoue, Hiromasa ; Shigyo, Mutsumi ; Takata, Shohei ; Hara, Nobuyuki. / Thromboxane causes airway hyperresponsiveness after cigarette smoke-induced neurogenic inflammation. In: Journal of Applied Physiology. 1996 ; Vol. 81, No. 6. pp. 2358-2364.
@article{0be5f02d39fb460da6785ba15be336cb,
title = "Thromboxane causes airway hyperresponsiveness after cigarette smoke-induced neurogenic inflammation",
abstract = "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.",
author = "Koichiro Matsumoto and Hisamichi Aizawa and Hiromasa Inoue and Mutsumi Shigyo and Shohei Takata and Nobuyuki Hara",
year = "1996",
month = "12",
doi = "10.1152/jappl.1996.81.6.2358",
language = "English",
volume = "81",
pages = "2358--2364",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "6",

}

TY - JOUR

T1 - Thromboxane causes airway hyperresponsiveness after cigarette smoke-induced neurogenic inflammation

AU - Matsumoto, Koichiro

AU - Aizawa, Hisamichi

AU - Inoue, Hiromasa

AU - Shigyo, Mutsumi

AU - Takata, Shohei

AU - Hara, Nobuyuki

PY - 1996/12

Y1 - 1996/12

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0030480647&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030480647&partnerID=8YFLogxK

U2 - 10.1152/jappl.1996.81.6.2358

DO - 10.1152/jappl.1996.81.6.2358

M3 - Article

C2 - 9018479

AN - SCOPUS:0030480647

VL - 81

SP - 2358

EP - 2364

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

IS - 6

ER -