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Related Experiment Video

Updated: Jul 14, 2026

Isolation of Rat Portal Fibroblasts by In situ Liver Perfusion

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.

Journal of Pediatric Surgery

|May 16, 2007

Summary

Extrahepatic portal vein obstruction (EHPVO) in rats led to reduced protein-C synthesis, not increased consumption. Liver repair responses were insufficient to maintain normal factor levels.

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Area of Science:

Hepatology
Vascular Surgery
Pediatric Gastroenterology

Background:

Extrahepatic portal vein obstruction (EHPVO) in children is associated with lower levels of liver-dependent coagulation factors.
The underlying mechanism for reduced factor levels in EHPVO remains unclear, with possibilities including diminished synthesis or increased consumption.

Purpose of the Study:

To develop a rat model of EHPVO to investigate the cause of decreased coagulation factor levels.
To test the hypothesis that reduced factor levels in EHPVO are due to diminished synthesis rather than increased consumption.

Main Methods:

A rat model of EHPVO was created by narrowing the portal vein (PV).
Liver and spleen mass, liver enzymes, coagulation parameters (prothrombin time, factor VII, protein-C), and hepatocyte proliferation/apoptosis were measured pre- and post-intervention.
Comparison was made between the experimental group (PV narrowing) and a sham-operated control group.

Main Results:

The EHPVO model successfully induced significant narrowing of the portal vein.
While liver mass remained unchanged, spleen mass increased proportionally in the experimental group.
Hepatocyte proliferation was significantly higher in the EHPVO group, indicating a repair response, but protein-C levels decreased significantly.

Conclusions:

The developed rat model effectively replicates PV narrowing seen in EHPVO.
Increased hepatocyte proliferation suggests a liver repair response to EHPVO.
This repair response is insufficient to maintain normal protein-C synthesis and serum levels in the EHPVO model.