好酸球性気管支炎の咳需容体感受性亢進のメカニズム

Material type: 文書・図像類

Author: 藤村, 政樹ほか

Publisher: -

Publication date: 1999-03-08

Material Format: Digital

Capacity, size, etc.: -

NDC: -

View All

Notes on use

Note (General)：: 金沢大学医学部付属病院1.慢性乾性咳嗽に関する臨床的研究(1)咳型喘息とは異なる新しい疾患概念として「アトピー咳嗽」を提唱した.(2)アトピー咳嗽では,気管支拡張薬は無効であり,メサコリン気道過敏性は正常であり,カプサイシンに対する気道の咳受容体感受性は亢進している.(3)アトピー咳嗽の組織学特徴は...

Related materials as well as pre- and post-revision versions

https://kaken.nii.ac.jp/search/?qm=90190066

https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-04807055/

https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-04807055/048070551994kenkyu_seika_hokoku_gaiyo/

Search by Bookstore

Holdings of Libraries in Japan

This page shows libraries in Japan other than the National Diet Library that hold the material.

List of Cooperating Institutions and Databases

Please contact your local library for information on how to use materials or whether it is possible to request materials from the holding libraries.

other

Kanazawa University Repository for Academic Resources
Digital
You can check the holdings of institutions and databases with which 学術機関リポジトリデータベース（IRDB）（機関リポジトリ） is linked at the site of 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）.
Kanazawa University Repository for Academic Resources

Search by Bookstore

Bibliographic Record

You can check the details of this material, its authority (keywords that refer to materials on the same subject, author's name, etc.), etc.

Digital

Material Type: 文書・図像類
Title: 好酸球性気管支炎の咳需容体感受性亢進のメカニズム
Author/Editor: 藤村, 政樹
Fujimura, Masaki
Author Heading: 藤村, 政樹
Fujimura, Masaki
Publication Date: 1999-03-08
Publication Date (W3CDTF): 1999-03-08
Alternative Title: Mechanisms of heightened airway cough receptor sensitivity in eosinophilic bronchitis (atopic cough : eosinophilic bronchitis without asthma).
Periodical title: 平成6(1994)年度科学研究費補助金一般研究(C) 研究成果報告書概要 = 1994 Fiscal Year Final Research Report Summary
No. or year of volume/issue: 1992 – 1994
Volume: 1992 – 1994
Pages: 3p.-
Text Language Code: jpn
Subject Heading: 慢性乾性咳嗽
病態生理
咳受容体感受性
気道過敏性
アトピー咳嗽
咳型喘息
好酸球性気管支炎
Chronic nonproductive cough
Pathophysiology
Cough receptor sensitivity
Bronchial responsiveness
Atopic cough
Cough variant asthma
Eosinophilic bronchitis
Target Audience: 一般
Note (General): 金沢大学医学部付属病院
1.慢性乾性咳嗽に関する臨床的研究(1)咳型喘息とは異なる新しい疾患概念として「アトピー咳嗽」を提唱した.(2)アトピー咳嗽では,気管支拡張薬は無効であり,メサコリン気道過敏性は正常であり,カプサイシンに対する気道の咳受容体感受性は亢進している.(3)アトピー咳嗽の組織学特徴は,以下の成績より中枢気道の好酸球性炎症であることが示唆される.すなわち,気管支肺胞洗浄液中には好酸球はみられず,気管支洗浄液中には好酸球はみられず,気管支生検組織には好酸球が僅かにみられ,高張食塩水吸入による誘導喀痰中には気管支喘息に匹敵する程度の好酸球がみられた.(4)アトピー咳嗽の治療には,ヒスタミンHI-拮抗薬とステロイド薬が有効である.2.好酸球性気管支炎に関する動物実験(1)モルモットにポリミキシンBを1回/週,3週間経鼻投与することによって,好酸球性気管支炎の作製に成功した.(2)本モデルでは,ヒスタミンに対する気道過敏性は亢進しておらず,カプサイシンに対する気道の咳受容体感受性は亢進していた.(3)ニューロペプチド受容体拮抗薬(FK-224)とトロンボキサン受容体拮抗薬(S-1452)は,本モデルの咳受容体感受性亢進を有意に抑制したが,β_2交感神経刺激薬(プロカテロール)は抑制しなかった.(4)ヒスタミンHI-拮抗薬(アゼラスチン)は本モデルの咳受容体感受性亢進を抑制した.3.結論以上の研究成績より,慢性乾性咳嗽(病的咳嗽)には少なくとも二つの病態があることが示された.すなわち,アトピー咳嗽では中枢気道の好酸球性炎症のよる咳受容体感受性亢進,咳型喘息では気道全体の好酸球性炎症による気道過敏性亢進に基づく気管支平滑筋の収縮である.
1.Clinical study on chronic nonproductive cough(1) A new clinical entity named as "ATOPIC COUGH" has been proposed, which is different from cough variant asthma.(2) Bronchodilator therapy is ineffective, bronchial responsiveness to methacholine is within normal range, and airway cough receptor sensitivity to inhaled capsaicin is heightened in atopic cough.(3) The histologic feature is considered to be large airway eosinophilic inflammation according to the following findings : no eosinophils in bronchoalveolar lavage fluid or bronchial lavage fluid, small number of eosinophils in biopsied bronchial specimens, and almost same number of eosinophils in hypertonic saline-induced sputum as bronchial asthma.(4) Histamine Hl-antagonists and steroids are effective for the treatment of atopic cough.2.Animal experiment on eosinophilic bronchitis(1) Eosinophilic bronchitis model of guinea pigs was successfully developed by intranasal administration of polymycin B twice a week for 3 weeks.(2) Airway cough receptor sensitivity to inhaled capsaicin was heightened but bronchial responsiveness to inhaled histamine was not increased in this model.(3) A neuropeptide inhibitor (FK-224) and a thromboxane receptor antagonist (S-1452) but not a beta2-agonist (procaterol) significantly reduced the heightened airway cough receptor sensitivity.(4) A histamine Hl-antagonist (azelastin) significantly suppressed the heightened airway cough receptor sensitivity.3.ConclusionFrom these results, it is suggested that there are at least 2 different mechanisms for the pathophysiology of persistent nonproductive cough (pathological cough) : heightened airway cough receptor sensitivity induced by eosinophilic inflammation of the large airway in atopic cough and bronchoconstriction based on bronchial hyperresponsiveness induced by eosinophilic inflammation of the central to peripheral airways in cough variant asthma.
研究課題/領域番号:04807055, 研究期間(年度):1992 – 1994
出典：研究課題「好酸球性気管支炎の咳需容体感受性亢進のメカニズム」課題番号04807055（KAKEN：科学研究費助成事業データベース（国立情報学研究所））（https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-04807055/048070551994kenkyu_seika_hokoku_gaiyo/）を加工して作成
DOI: 10.24517/00066884
Source: https://kanazawa-u.repo.nii.ac.jp/?action=repository_action_common_download&item_id=60637&item_no=1&attribute_id=26&file_no=1
https://kanazawa-u.repo.nii.ac.jp/?action=repository_action_common_download&item_id=60637&item_no=1&attribute_id=26&file_no=1
Access Restrictions: 限定公開
Rights (production): CC BY-NC-ND
Related Material: https://kaken.nii.ac.jp/search/?qm=90190066
https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-04807055/
https://kaken.nii.ac.jp/ja/report/KAKENHI-PROJECT-04807055/048070551994kenkyu_seika_hokoku_gaiyo/
Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）
https://irdb.nii.ac.jp
Original Data Provider (Database): 金沢大学 : 金沢大学学術情報リポジトリKURA