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Updated: Jul 14, 2026

Isolation of Rat Portal Fibroblasts by In situ Liver Perfusion
Published on: June 29, 2012
Extrahepatic portal vein obstruction results in hepatocyte proliferation but a decrease in protein-C synthesis
Bill Chiu1, Hector Melin-Aldana, Srikumar Pillai
1Department of Surgery, Children's Memorial Hospital, Northwestern University Feinberg School of Medicine, Chicago, IL 60614, USA.
Purpose:
Extrahepatic portal vein obstruction (EHPVO) results in decreased levels of liver-dependent coagulation factors in children. We developed a rat model to test the hypothesis that lower factor levels associated with EHPVO were from diminished synthesis rather than increased consumption.
Methods:
A total of 8 rats (experimental group) underwent narrowing of portal vein (PV) and 8 underwent sham operations. Liver and spleen mass, serum alanine aminotransferase, bilirubin, ammonia, prothrombin time, factor VII, and protein-C were measured before and 3 months after PV narrowing. Hepatocyte proliferation and apoptosis were quantified using Ki-67 and TUNEL assays.
Results:
Portal vein diameter was 71% +/- 13% narrower in experimental animals. Liver mass was unchanged, but proportional spleen mass was higher in the experimental group at 3 months (0.31% +/- 0.05% vs 0.26% +/- 0.04%; P < .05). Percent apoptotic cells at 3 months was similar in both groups (0.14% +/- 0.08% vs 0.13% +/- 0.07%), but percent proliferating cells was higher in the experimental group (0.63% +/- 0.17% vs 0.34% +/- 0.11%; P < .05). Three-month protein-C levels decreased significantly only in the experimental group compared with preoperative values (12.8% +/- 4.4% vs 7.6% +/- 5.1%; P < .05). Changes in other parameters were not significant.
Conclusions:
Our EHPVO model consistently produced PV narrowing. The increase in hepatocyte proliferation seen after EHPVO suggests a liver repair response that is insufficient to maintain normal protein-C synthesis and serum levels.
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