ログイン
言語:

WEKO3

  • トップ
  • ランキング
To
lat lon distance
To

Field does not validate



インデックスリンク

インデックスツリー

メールアドレスを入力してください。

WEKO

One fine body…

WEKO

One fine body…

アイテム

  1. Public
  2. 研究紀要
  3. 医学雑誌
  4. 19(1)1994

閉塞性黄疸時の内因性エンドトキシン血症ラットにおけるウルソデオキシコール酸静脈内投与の効果について

https://kindai.repo.nii.ac.jp/records/2002006
https://kindai.repo.nii.ac.jp/records/2002006
9f0bc1e6-23bb-49d2-84c0-721a702af9ec
名前 / ファイル ライセンス アクション
AN00063584-19940325-0109.pdf AN00063584-19940325-0109.pdf (482.8 KB)
Item type ☆紀要論文 / Departmental Bulletin Paper(1)
公開日 2024-11-15
タイトル
タイトル 閉塞性黄疸時の内因性エンドトキシン血症ラットにおけるウルソデオキシコール酸静脈内投与の効果について
言語 ja
タイトル
タイトル The protective effect of the intravenous administration of ursodeoxycholic acid against endogenous endotoxemia in obstructive jaundiced rats
言語 en
著者 中谷, 公一

× 中谷, 公一

ja 中谷, 公一
近畿大学

en Nakatani, Masakazu
Kinki University

Search repository
言語
言語 jpn
キーワード
主題 obstructive jaundice, endotoxin, endogenous endotoxemia, ursodeoxycholic acid, bacterial translocation, fluorescein isothiocyanate
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 19, 号 1, p. 109-118, 発行日 1994-03-25
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 Endogenous endotoxemia, which is due to the facilitated bacterial translocation from intraluminal space of the gastrointestinal tract to portal vein in spite of the absence of a focus of infection, is possibly involved in poor biliary drainage of percutaneous transhepatic cholangiodrainage (PTCD) in the case of obstructive jaundice. Ursodeoxycholic acid (UDCA) is a bile acid, which is often orally used in the treatment of cholestasis. Herein, the protective effect of intravenous administration of UDCA against endotoxemia was determined by measuring the survival rate, endotoxin concentration in portal and peripheral veins, ATP content of rat liver and serum level of TNF-α. Endogenous endotoxemia in rats with obstructive jaundice induced by simultaneous administration of E. coli endotoxin orally at the dose of 5 mg/100 g body weight and lead acetate intravenously at the dose of 5 mg/100 g body weight following bile duct ligation for two weeks and recanaliculization thereafter according to the model of Bailey. UDCA administration at the dose of 0.05 μmol/100 g body weight/min improved the survival rate significantly. In the UDCA-treated group, the endotoxin concentration in the peripheral vein was significantly lower and ATP content was significantly recovered to the normal level. Conversely, the endotoxin concentration in the portal vein and serum level of TNF-α were not different between the UDCA-treated and saline-treated control rats. To investigate the mechanism of effect of UDCA on the secretion of endotoxin into bile, fluorescein isothiocyanate (FITC) labeled lipopolysaccharide (LPS) was administered via the portal vein and its concentration in bile was measured with a spectrophotofluorometer. A significant increase in the secretion of LPS into the bile was noticed in UDCA-treated rats, suggesting that the lower concentration of LPS in the peripheral vein in UDCA-treated rats depends on the increase in secretion of LPS into the bile. These findings demonstrate that intravenous administration of UDCA protects against endotoxemia in obstructive jaundice by activating the transport pathway of endotoxin across the hepatocytes into the bile but has no effect on Kupffer cells. Therefore, UDCA treatment may be beneficial in the case of poor biliary drainage of PTCD in obstructive jaundice.
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
戻る
0
views
See details
Views

Versions

Ver.1 2024-11-15 00:50:44.169317
Show All versions

Share

Mendeley Twitter Facebook Print Addthis

Cite as

エクスポート

OAI-PMH
  • OAI-PMH JPCOAR 2.0
  • OAI-PMH JPCOAR 1.0
  • OAI-PMH DublinCore
  • OAI-PMH DDI
Other Formats
  • JSON
  • BIBTEX

Confirm


Powered by WEKO3


Powered by WEKO3