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. 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 (AT III) on leukocyte kinetics and liver damage. METHODS: Hepatic and intestinal microcirculation were 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 AT III. 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 (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 AT III 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 AT Ⅲ.