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実験気管支喘息モデルにおける気道過敏性亢進発症機序に関する検討：β-adrenergic receptorとoxygen radicalに関する実験的観察
https://kindai.repo.nii.ac.jp/records/2002203
https://kindai.repo.nii.ac.jp/records/2002203205164a5-7c3f-478a-8fb8-ec640acfeed4
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
AN00063584-19930625-0213.pdf (1.9 MB)
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| Item type | ☆紀要論文 / Departmental Bulletin Paper(1) | |||||||||
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| 公開日 | 2024-12-20 | |||||||||
| タイトル | ||||||||||
| タイトル | 実験気管支喘息モデルにおける気道過敏性亢進発症機序に関する検討：β-adrenergic receptorとoxygen radicalに関する実験的観察 | |||||||||
| 言語 | ja | |||||||||
| タイトル | ||||||||||
| タイトル | Role of β-adrenergic receptors and oxygen radicals in the mechanism of bronchial hyperresponsiveness in an experimental model of bronchial asthma | |||||||||
| 言語 | en | |||||||||
| 著者 |
寺本, 和弘
× 寺本, 和弘
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| 言語 | ||||||||||
| 言語 | jpn | |||||||||
| キーワード | ||||||||||
| 主題 | bronchial asthma, β-adrenergic receptor bronchial hyperresponsiveness, autoradiography, oxygen radical, superoxide dismutase | |||||||||
| 資源タイプ | ||||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||||
| 資源タイプ | departmental bulletin paper | |||||||||
| 出版タイプ | ||||||||||
| 出版タイプ | AM | |||||||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||||||
| 出版者 名前 | ||||||||||
| 出版者 | 近畿大学医学会 | |||||||||
| 言語 | ja | |||||||||
| bibliographic_information |
ja : 近畿大学医学雑誌 en : Medical Journal of Kinki University 巻 18, 号 2, p. 213-232, 発行日 1993-06-25 |
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| ISSN | ||||||||||
| 収録物識別子タイプ | PISSN | |||||||||
| 収録物識別子 | 03858367 | |||||||||
| 内容記述 | ||||||||||
| 内容記述タイプ | Abstract | |||||||||
| 内容記述 | In this study, ^<125>I-Iodocyanopindolol radioligand binding studies using tissue homogenates found no relationship between the β-adrenergic receptor number and % changes in tidal volume (V_T) after ovalbumin (OA) inhalation. However, techniques using tissue homogenates do not allow precise anatomic localization of pulmonary β-adrenergic receptors or identification of the sites. Therefore that was investigated using the autoradiographic method. To clarify the anatomic distribution and density, an experimental model of bronchial asthma was prepared. The first group of animals was sensitized to OA (OA). The second group of animals was sacrified after a single challenge by OA inhalation (BA1). The third group of animals was sacrified after three inhalation challenges (BA3). The fouth group of animals was sacrified after twelve inhalation challenges (BA12). The majority of β-receptors were localized in the alveolar epithelium. A significant decrease in β-receptor density was observed in all pulmanary sites in OA, BA1, and BA3 animals. Although significant increase was observed in the alveolar epithelium in BA12 and the total number of β-receptors from radioligand binding studies was also significantly increased, significant decrease was observed in the bronchiolar muscle. Therefore, it was considered that an asthma attack occurred in BA12. β-receptor number in bronchiolar smooth muscle only accounted for the changes in pulmonary function. However, airway inflammation is thought to be an important pathologic factor in bronchial asthma. Stimulated inflammatory cells themselves release reactive oxygen compounds such as superoxide and hydrogen peroxide as well as other chemical mediaters. The effects of reactive oxygen compounds on airway smooth muscle have been reported, including direct effects on muscle tone and alterations of receptor-mediated responses. We investigated oxygen radicals and superoxide dismutase, which is an oxygen radical scavenger. In sensitized animals, both oxygen radicals and superoxide dismutase were significantly increased. We also studied the effects of preteatment with diethyldithiocarbamate, which inhibits superoxide dismutase. The duration of asthma attack was significantly prolonged by pretreatmant. These data support the concept that oxygen radicals induce airway hyperresponsiveness. Furthermore, we investigated the relationship between β-adrenergic receptors and oxygen radicals. Pretreatment with terbutaline sulfate significantly decreased integral values of luminol dependent chemiluminescence. Therefore, the expression of β-adrenergic receptors may be related to oxygen radicals in allergic inflammation. | |||||||||
| 言語 | en | |||||||||
| 内容記述 | ||||||||||
| 内容記述タイプ | Other | |||||||||
| 内容記述 | 本文データはCiNiiから複製したものである。 | |||||||||
| 言語 | ja | |||||||||
