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Background & Aims  To determine the pathogenesis of liver nodules, and lesions similar to obliterative portal venopathy, observed after portosystemic shunts or portal vein thrombosis in humans.    Methods  We conducted an experimental study comparing portacaval shunt (PCS), total portal vein ligation (PVL), and sham (S) operated rats. Each group were either sacrificed at 6 weeks (early) or 6 months (late). Arterial liver perfusion was studied in vivo using CT, and histopathological changes were noted. Liver mRNA levels were quantified by RT-QPCR for markers of inflammation ( Il10 ,  Tnfa ), proliferation ( Il6st ,  Mki67 ,  Hgf ,  Hnf4a ), angiogenesis: ( Vegfa ,  Vegfr 1 ,  2  and  3; Pgf ), oxidative stress ( Nos2 , and  3 ,  Hif1a ), and fibrosis ( Tgfb ). PCS and PVL were compared to the S group.    Results  Periportal fibrosis and arterial proliferation was observed in late PCS and PVL groups. CT imaging demonstrated increased arterial liver perfusion in the PCS group. RT-QPCR showed increased inflammatory markers in PCS and PVL early groups.  Tnfa  and  Il10  were increased in PCS and PVL late groups respectively. All proliferative markers increased in the PCS, and  Hnf4a  in the PVL early groups.  Mki67 and Hnf4a  were increased in the PCS late group.  Nos3  was increased in the early and late PCS groups, and  Hif1a  was decreased in the PVL groups. Markers of angiogenesis were all increased in the early PCS group, and  Vegfr3 and Pgf  in the late PCS group. Only  Vegfr3  was increased in the PVL groups.  Tgf  was increased in the PCS groups.    Conclusions  Portal deprivation in rats induces a sustained increase in intrahepatic markers of inflammation, angiogenesis, proliferation, and fibrosis.

plos one

Hepatic Proliferation and Angiogenesis Markers Are Increased after Portal Deprivation in Rats: A Study of Molecular, Histological and Radiological Changes