AJP - Gastrointestinal and Liver Physiology, Vol 270, Issue 5 804-G812, Copyright © 1996 by American Physiological Society
Bile secretion in rats with indomethacin-induced intestinal inflammation
T. Yamada, M. Hoshino, T. Hayakawa, Y. Kamiya, H. Ohhara, K. Mizuno, H. Yamada, T. Nakazawa, T. Inagaki, A. Uchida, M. Miyaji and T. Takeuchi
First Department of Internal Medicine, Nagoya City University Medical School, Aichi, Japan.
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, alpha- and beta-muricholic acids were significantly deceased 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 function was maintained in
this model.
