Bile secretion in rats with indomethacin-induced intestinal
inflammation.
Yamada, Tamaki, Makoto Hoshino, Tomihiro Hayakawa,yasutaka Kamiya,
Hirotaka Ohhara, Kiyoshi Mizuno, Hisashi Yamada,takahiro Nakazawa,
Takanori Inagaki, Atsuo Uchida, Makoto Miyaji, and Toshihiko
Takeuchi.
First Department of Internal Medicine, Nagoya City University
Medical School, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Aichi,
Japan
APStracts 2:0264G, 1995.
The objective of this study was to characterize the bile secretion,
including the composition of biliary bile acids, bile salt pool size,
and transcytotic vesicle transport, in a rat model of subacute
intestinal inflammation induced by indomethacin. Indomethacin
treatment significantly decreased bile acid-independent bile flow and
biliary secretion of bile acid and cholesterol, while increasing
biliary phospholipid output in vivo. Although indomethacin treatment
did not change the bile salt pool size in vivo, [circumflex]a - and
[circumflex]a -muricholic acids were significantly decreased and
hyodeoxycholic and deoxycholic acids were increased in bile. Bile
flow and the transport maximum of taurocholate did not decrease and
biliary horseradish peroxidase output was significantly enhanced in
isolated perfused livers from indomethacin-treated rats. Endotoxin in
the portal blood was significantly increased in rats treated with
indomethacin. Clindamycin slightly reduced intestinal inflammation
but significantly prevented decreases in bile flow, bile acid output,
and transport maximum of taurocholate. We conclude that although
biliary secretory function was apparently decreased in vivo that of
hepatocyte was maintained in this model.
Received 3 October 1995; accepted in final form 11 November 1995.
APS Manuscript Number G428-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 December 95