Evaluation of hemodynamics and hepatic mitochondrial function on extrahepatic portal obstruction in the rat.

An animal model resembling clinical cases with extrahepatic portal vein obstruction was developed. The changes in hepatic mitochondrial function and the hepatic hemodynamics including hepatic regional blood flow, portal venous pressure, and portogram were evaluated to assess the effect of portal vein obstruction in the model. Portal vein ligation in this model was a simple and easy maneuver and could produce collateral veins to the liver--cavernomatous transformation--which were obviously seen in clinical patients with extrahepatic portal obstruction. Hepatic blood flow was significantly decreased until 5 days after portal vein ligation; however, hepatic blood flow was gradually increased and reached the normal value at 3 weeks after portal vein ligation due to the formation of the collateral veins to the liver. Respiratory parameters of mitochondria were gradually decreased and reached the lowest levels at 5 days after portal vein ligation, while they recovered to normal values in accordance with increasing hepatic blood flow at 3 weeks after portal vein ligation. In extrahepatic portal obstruction, although the liver is temporarily deteriorated by portal vein obstruction such as portal vein thrombosis, hepatic blood flow and the liver functions are to be normally improved with the formation of collateral veins to the liver.