Chest ACCP Education Calendar
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
This Article
Right arrow Full Text Free
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via ISI Web of Science (3)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Teramoto, S.
Right arrow Articles by Abe, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Teramoto, S.
Right arrow Articles by Abe, S.
(Chest. 2003;123:524-529.)
© 2003 American College of Chest Physicians

Neurokinin-1 and Neurokinin-2 Antagonism Inhibits Long-term Acid Fog-Induced Airway Hyperresponsiveness*

Shin Teramoto, MD; Hiroshi Tanaka, MD; Satoshi Kaneko, MD and Shosaku Abe, MD

* From the Third Department of Internal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.

Correspondence to: Shin Teramoto, MD, Third Department of Internal Medicine, Sapporo Medical University School of Medicine, South-1, West-16, Chuo-ku, Sapporo, 060-8543, Japan; e-mail: teramoto{at}sapmed.ac.jp

Background: We recently reported that airway hyperresponsiveness (AHR) induced by a 6-h exposure to sulfuric acid (H2SO4) was inhibited by either the neurokinin (NK)-1 receptor antagonist, FK888, or the NK-2 receptor antagonist, SR48968, when administered immediately before the exposure. The aims of this study were to determine whether these antagonists have any therapeutic efficiency against AHR after long-term H2SO4 inhalation and to elucidate the mechanisms in ovalbumin sensitized guinea pigs.

Methods: Specific airway resistance (sRaw), AHR, and BAL fluid were analyzed after an 8-week exposure to H2SO4 aerosol (82 mg/m3, pH 1.7, 40 mOsm) or hypotonic saline solution (pH 5.9, 40 mOsm) as a control. The H2SO4 group then received a 2-week treatment with FK888, SR48968, or vehicle.

Results: The AHR and the eosinophil count in BAL fluid were significantly increased in the H2SO4 group compared to control animals, while sRaw was significantly elevated in both groups after the 8-week exposure. Treatment with both FK888 and SR48968 significantly reduced the AHR and tended to inhibit eosinophilia in BAL fluid, but sRaw did not change. The degree of AHR improvement with SR48968 was much larger than with FK888.

Conclusion: Our results show that both NK-1 and NK-2 receptor antagonists inhibited long-term H2SO4-induced AHR in sensitized guinea pigs, and the effect was much greater with an NK-2 antagonist. We suggest that NK-1 or NK-2 antagonism might partially inhibit the H2SO4-induced influx of eosinophils into the lung.

Key Words: acid fog • asthma • neurokinin-1 receptor • neurokinin-2 receptor • sulfuric acid






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2003 by the American College of Chest Physicians.