OBJECTIVE: : The present study was conducted to elucidate the sequential alterations in the hepatic microvascular inflammatory response to extrahepatic biliary obstruction. METHODS: : The hepatic microvasculature in anesthetized Sprague-Dawley rats was studied by in vivo microscopy 3, 7, and 14 days after bile duct ligation (BDL) or sham operation. RESULTS: : The numbers of adhering leukocytes and swollen sinusoidal endothelial cells were significantly increased at 3, 7, and 14 days after BDL when compared with sham-operated controls. Concomitantly, the numbers of sinusoids containing blood flow were significantly and progressively decreased by up to 30%. The phagocytic activity of hepatic macrophages was significantly elevated during the development of biliary cholestasis. In particular, centrilobular phagocytosis at 14 days after BDL was significantly increased 1.4- to 2.0-fold when compared with that at 3 and 7 days after BDL. Electron microscopy also revealed evidence of activated Kupffer cells reflected by numerous filopodia and ruffles. CONCLUSIONS: : These results suggest that hepatic microcirculatory dysfunction subsequent to BDL contributes to cholestatic liver injury. Microcirculation (2003) 10, 421-432. doi:10.1038/sj.mn.7800208
OBJECTIVE: : The present study was conducted to elucidate the sequential alterations in the hepatic microvascular inflammatory response to extrahepatic biliary obstruction. METHODS: : The hepatic microvasculature in anesthetized Sprague-Dawley rats was studied by in vivo microscopy 3, 7, and 14 days after bile duct ligation (BDL) or sham operation. RESULTS: : The numbers of adhering leukocytes and swollen sinusoidal endothelial cells were significantly increased at 3, 7, and 14 days after BDL when compared with sham-operated controls. Concomitantly, the numbers of sinusoids containing blood flow were significantly and progressively decreased by up to 30%. The phagocytic activity of hepatic macrophages was significantly elevated during the development of biliary cholestasis. In particular, centrilobular phagocytosis at 14 days after BDL was significantly increased 1.4- to 2.0-fold when compared with that at 3 and 7 days after BDL. Electron microscopy also revealed evidence of activated Kupffer cells reflected by numerous filopodia and ruffles. CONCLUSIONS: : These results suggest that hepatic microcirculatory dysfunction subsequent to BDL contributes to cholestatic liver injury. Microcirculation (2003) 10, 421-432. doi:10.1038/sj.mn.7800208
Authors: Eline Vanheule; Anja M Geerts; Jacques Van Huysse; Daphné Schelfhout; Marleen Praet; Hans Van Vlierberghe; Martine De Vos; Isabelle Colle Journal: Int J Exp Pathol Date: 2008-12 Impact factor: 1.925
Authors: Stefan Dold; Matthias W Laschke; Yilin Zhau; Martin Schilling; Michael D Menger; Bengt Jeppsson; Henrik Thorlacius Journal: Inflamm Res Date: 2009-10-15 Impact factor: 4.575