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内因性線溶に関する研究 : 活性化と阻害について
https://hsuh.repo.nii.ac.jp/records/7740
https://hsuh.repo.nii.ac.jp/records/774008eb97bb-ccc5-46ce-ab2d-263e06dacf65
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
内因性線溶に関する研究 : 活性化と阻害について (1.9 MB)
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| Item type | 紀要論文(ELS) / Departmental Bulletin Paper(ELS)(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 1992-06-30 | |||||
| タイトル | ||||||
| タイトル | 内因性線溶に関する研究 : 活性化と阻害について | |||||
| 言語 | ja | |||||
| タイトル | ||||||
| タイトル | Studies on Intrinsic Fibrinolysis: Activation and Inhibition | |||||
| 言語 | en | |||||
| 言語 | ||||||
| 言語 | jpn | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | intrinsic fibrinolysis | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | contact activation | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | coagulation Factor XII | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | C1-inhibitor | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | prekallikrein. | |||||
| 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 | |||||
| ページ属性 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | P(論文) | |||||
| 言語 | ja | |||||
| 記事種別(日) | ||||||
| ja | ||||||
| 原著 | ||||||
| 記事種別(英) | ||||||
| en | ||||||
| ORIGINAL ARTICLE | ||||||
| 著者名(日) |
佐藤, 雅寛男
× 佐藤, 雅寛男 |
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| 著者所属(日) | ||||||
| ja | ||||||
| 東日本学園大学歯学部内科学講座 | ||||||
| 著者所属(英) | ||||||
| en | ||||||
| Department of Internal Medicine, School of Dentistry, HIGASHI-NIPPON-GAKUEN UNIVERSITY | ||||||
| 抄録(英) | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | The activation of coagulation Facor XII results in initiation of the intrinsic fibrinolysis. This study was carried out to clarify what promoting and inhibitory factors are related to the process. (1) Promotion (1) In vitro : The fibrionlytic activities were determined by the contact activation of Factor XIIH with four reagents, kaolin, dextran sulphate, ellagic acid and celite. Kaolin showed the strongest effect on increasing in fibrinolysis, which was caused via prekallikrein, namely Factor XII dependent pathway. Though the potency of dextran sulphate to activate prekallikrein was weak, but it enhanced the fibrinolysis independently of Factor XII. (2) In vivo : No contact activating reagent to use in man was available, so any experiment was not done. (2) Inhibition (1) In vitro: It is known that contact factors (Factor XII, Factor XI, prekallikrein and high molecular weight kininogen as cofactors) are under the regulation of C1-inhibitor. To investigate the role of C1-inhibitor in regulation of the intrinsic fibrinolysis, normal healthy subjects and a patient of hereditary angioneurotic edema were examined. By the innactivation of C1-inhibitor, using its blocking reagent, flufenamate, normal plasma showed an increase in fibrinolysis. In plasma of a patient of hereditary angioneurotic edema, conversion of prekallikrein to kallikrein was easily occurred and the fibrinolytic activity was very high with or without activating reagents. (2) In vivo: At the point of view that C1-inhibitor regulates the intrinsic fibrinolysis, flufenamate was administrated in three healthy subjects. They showed an enhancement of fibrinolysis and prekallikrein activation by the administration. It is the first report to recognize the manifestation of the intrinsic fibrinolysis in vivo, by the method of innactivation of C1-inhibitor. It is suggested that Factor XII plays an important role in the initiation of rather the fibrinolytic system than the coagulation system. | |||||
| 言語 | en | |||||
| 雑誌書誌ID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AN0008135X | |||||
| 書誌情報 |
ja : 東日本歯学雑誌 巻 11, 号 1, p. 1-16, 発行日 1992-06-30 |
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| 出版タイプ | ||||||
| 出版タイプ | VoR | |||||
