Brief Reports
Copyright ©The Author(s) 2005. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Aug 28, 2005; 11(32): 4997-5001
Published online Aug 28, 2005. doi: 10.3748/wjg.v11.i32.4997
Impact of antithrombin III on hepatic and intestinal microcirculation in experimental liver cirrhosis and bowel inflammation: An in vivo analysis
Sasa-Marcel Maksan, Zilfi Ülger, Martha Maria Gebhard, Jan Schmidt
Sasa-Marcel Maksan, Department of Surgery, University of Mainz, Germany
Zilfi Ülger, Martha Maria Gebhard, Jan Schmidt, Department of Surgery, University of Heidelberg, Germany
Author contributions: All authors contributed equally to the work.
Correspondence to: Sasa-Marcel Maksan, MD, Department of Surgery, University of Mainz, Langenbeckstrasse 1, Mainz D-55131, Germany. maksan@ach.klinik.uni-mainz.de
Telephone: +49-6131-171
Received: October 29, 2004
Revised: November 20, 2004
Accepted: November 23, 2004
Published online: August 28, 2005
Abstract

AIM: To analyze the hepatic and intestinal microcirculation in an animal model of liver cirrhosis and inflammatory bowel disease (IBD) and to characterize the anti-inflammatory action of antithrombin III (ATIII) on leukocyte kinetics and liver damage.

METHODS: Hepatic and intestinal microcirculation was investigated by intravital videomicroscopy. Standardized models of experimental chronic liver cirrhosis and bowel inflammation were employed. Animals were divided into four groups (n = 6/group): controls, animals with cirrhosis, animals with cirrhosis and IBD, animals with cirrhosis and IBD treated with ATIII.

RESULTS: Cirrhosis facilitated leukocyte rolling and sticking in hepatic sinusoids (1.91±0.28 sticker/µm vs 0.5±0.5 sticker/µm in controls, P<0.05). The effect enhanced in animals with cirrhosis and IBD (5.4±1.65 sticker/µm), but reversed after ATIII application (3.97±1.04 sticker/µm, P<0.05). Mucosal blood flow showed no differences in cirrhotic animals and controls (5.3±0.31 nL/min vs 5.4±0.25 nL/min) and was attenuated in animals with cirrhosis and IBD significantly (3.49±0.6 nL/min). This effect was normalized in the treatment group (5.13±0.4 nL/min, P<0.05). Enzyme values rose during development of cirrhosis and bowel inflammation, and reduced after ATIII application (P<0.05).

CONCLUSION: Liver cirrhosis in the presence of IBD leads to a significant reduction in mucosal blood flow and an increase in hepatic leukocyte adherence with consecutive liver injury, which can be prevented by administration of ATIII.

Keywords: Liver cirrhosis; Microcirculation; Bowel inflammation; Liver; Antithrombin III