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The objective of this study was to develop an easy and simple experimental rat model of total hepatectomy, hepatic ischemia and extrahepatic portal obstruction. The first operation involved transposing the spleen with its scarified capsule in a subcutaneous pouch to produce portasystemic anastomosis. Total hepatectomy was easily performed in a lobe-by-lobe fashion 2 weeks following the first stage operation. Anhepatic rats receiving a glucose infusion survived for about 10 hours and all died of acute hepatic failure. Hepatic support systems can be accurately evaluated in this anhepatic rat model because of its uniformity. Sixty minutes of hepatic ischemia was able to be performed in rats with a transposed spleen for a portasystemic shunt and no complicated or technically involved procedure was required for the ischemic model. No rats died due to technical difficulties, suggesting the reliability and reproducibility of this ischemic model. An animal model resembling extrahepatic portal vein obstruction was also obtained by ligation of the portal vein; a simple maneuver which was able to produce collateral veins to the liver and cavernous transformation, as similarly seen in clinical patients with extrahepatic portal obstruction. Because these 3 animal models were so easily achieved in the rat, and since the changes in hepatic function and formation of the collaterals to the liver after portal vein occlusion are still poorly understood, this model should prove valuable for future study.

Obstructive jaundice model was created using rats by the ligation of bile duct. One, 2, 3 weeks later, the respiratory function and morphology of the hepatic mitochondria were comparatively evaluated between mitochondria directly fractionated from liver tissue and mitochondria from isolated hepatocytes. Respiratory function of the former deteriorated with the duration of jaundice. ATP synthesis decreased to 75% of the control at 1 and 2 weeks, and 58% at 3 weeks after ligation. On the contrary, it was 97%, 88% and 87% of the control. On the contrary, it was 97%, 88% and 87% of the control at 1, 2 and 3 weeks in the latter. By electron microscopic examination, the size of mitochondria of the jaundiced liver is inconsistent and smaller in general than the control. These data suggest that the deterioration of mitochondrial function in the jaundiced liver is not caused mainly by the disturbance of mitochondria themselves, but caused by the respiratory inhibitory factors which exist around the mitochondria.