Mechanical approach of some liver diseases and their impact on hemodynamics.

The hepatic circulatory system consists of two inflow vascular networks -the hepatic artery (HA) and the portal vein (PV)-, liver capillaries (sinusoids), and an outflow network formed by the hepatic veins. We present novel mechanical models of non-alcoholic fatty liver disease (NAFLD) and congestive hepatopathy (CH), building on our 1D healthy liver circulation model that considers vessel wall elasticity and pulsatile blood flow and pressure. NAFLD is emulated by modeling sinusoids compressed by fat-laden hepatocytes (reducing their cross-sectional area), and adopting NAFLD-reported wall elasticity. This leads to a moderate increase in sinusoids inlet pressure (portal hypertension) that grows with steatosis grade but remains clinically insignificant, consistent with observations in NAFLD patients without advanced fibrosis or cirrhosis. Regarding microcirculation, blood flow decreases in fatty sinusoids and increases in healthy ones, with larger variations at higher steatosis grades. CH is modeled in two stages. In stage 1, the inferior vena cava (IVC) pressure is increased, which propagates upstream producing the largest pressure rise at sinusoids inlet, and reducing PV and HA inflows. As HA inflow reduction is minimal, the decrease in total hepatic inflow is mainly driven by diminished portal flow due to the reduced pressure gradient between portal inflow and the IVC. In stage 2, reduced hepatic inflow combined with fibrotic and thrombotic sinusoids-modeled by decreasing their cross-sectional area and using CH-reported stiffness-further increases sinusoidal pressure. Despite portal hypertension, the portal pressure gradient remains within healthy limits due to elevated hepatic outflow pressure, consistent with clinical observations.