UNLABELLED: The aim is to evaluate the liver damage due to an experimental animal model based in the temporal obstruction of biliar extrahepatic duct and determine the relation between obstruction and severity of damage through time. METHODS: We used 20 adults male mice going from 25 to 35 g weight, previous to general anesthesia, a surgical incision was applied and biliar duct were localized and tied using linen cloth. Six animals were sacrificed each time at 1, 7 and 15 days of treatment, the hepatic, lung, kidney, hearth and brain were obtained for histopatologic analysis using optic microscope. RESULTS: In the first day 20% of hepatic samples, light lesions as sinusoidal congestion and dilation of portal vessel with hepatocelular biliar stasis were found. In 7th day additional lesions were found as accumulations of biliar pigments in the cholangiols, proliferation of portal collagens and light pericholangiolar proliferation in 60% of samples. At 15th day, severely lesions as hamartomatous proliferation of cholangiols and portal fibrosis of biliar ducts that deformed the boundary plaque and lobular in 15% of samples. In brain, hearth, and lung samples showed vascular dilation and severe congestion, except at 15th day, when samples of kidneys showed biliar pigment precipitation in lumen of collets ducts. CONCLUSIONS: The proposed method is useful to study the chronologic relationship of anatomophatologic damage produced by biliar obstruction.
UNLABELLED: The aim is to evaluate the liver damage due to an experimental animal model based in the temporal obstruction of biliar extrahepatic duct and determine the relation between obstruction and severity of damage through time. METHODS: We used 20 adults male mice going from 25 to 35 g weight, previous to general anesthesia, a surgical incision was applied and biliar duct were localized and tied using linen cloth. Six animals were sacrificed each time at 1, 7 and 15 days of treatment, the hepatic, lung, kidney, hearth and brain were obtained for histopatologic analysis using optic microscope. RESULTS: In the first day 20% of hepatic samples, light lesions as sinusoidal congestion and dilation of portal vessel with hepatocelular biliar stasis were found. In 7th day additional lesions were found as accumulations of biliar pigments in the cholangiols, proliferation of portal collagens and light pericholangiolar proliferation in 60% of samples. At 15th day, severely lesions as hamartomatous proliferation of cholangiols and portal fibrosis of biliar ducts that deformed the boundary plaque and lobular in 15% of samples. In brain, hearth, and lung samples showed vascular dilation and severe congestion, except at 15th day, when samples of kidneys showed biliar pigment precipitation in lumen of collets ducts. CONCLUSIONS: The proposed method is useful to study the chronologic relationship of anatomophatologic damage produced by biliar obstruction.