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Functional shift with maintained regenerative potential following portal vein ligation
Tibor Kovács1, Domokos Máthé2,3, András Fülöp1
1Hepato-Pancreatico-Biliary Surgery Research Center Hungary, 1st Department of Surgery, Semmelweis University, Budapest, Hungary.
Scientific Reports
|December 24, 2017
Summary
Selective portal vein ligation (PVL) causes liver lobe atrophy and hypertrophy. Despite temporary transport function decline, the non-ligated lobe compensates, preserving overall liver function for tumor resection.
Area of Science:
- Hepatology
- Surgical Oncology
- Physiology
Background:
- Selective portal vein ligation (PVL) is a strategy for two-stage liver resection of unresectable tumors.
- PVL induces atrophy in ligated lobes and hypertrophy in non-ligated lobes, necessitating functional assessment.
Purpose of the Study:
- To characterize in vitro and in vivo liver function alterations following PVL.
- To evaluate the morpho-functional changes in both portally ligated (LL) and non-ligated lobes (NLL).
Main Methods:
- In vivo studies in Wistar rats (n=106) at multiple time points post-PVL.
- Magnetic resonance imaging (MRI) for lobe volume, in vitro hepatocyte function assays, immunohistochemistry, and in vivo functional imaging (ICG, HBS, CLE).
Main Results:
- PVL induced the expected atrophy-hypertrophy complex.
- Bilateral, temporary reductions in bile acid and bilirubin transport were observed.
- While LL function showed permanent involution, NLL function recovered excessively, restoring overall liver transport capacity.
Conclusions:
- Functioning hepatocytes persist in the atrophied lobe post-PVL.
- The hypertrophied NLL compensates for functional deficits, highlighting the importance of assessing liver functional reserve.
