Evidence map›Paper›PMID 42171825›Full record

ArticleBiomechanics and modeling in mechanobiology2026

Lumped parameter modeling of changes in liver hemodynamics due to cirrhosis.

Edith Luveina Joseph, Himanshi Saini, Usha Kini, Timothy L Pruett, Joseph Sushil Rao, Jeffrey Tithof

Abstract read
In one paragraph

Article in Biomechanics and modeling in mechanobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Edith Luveina Joseph *Department of Mechanical Engineering, University of Minnesota, 111 Church St SE, Minneapolis, Minnesota, 55455, USA.
Himanshi Saini *Department of Mechanical Engineering, University of Minnesota, 111 Church St SE, Minneapolis, Minnesota, 55455, USA.
Usha KiniDepartment of Pathology, St. John's National Academy of Health Sciences, Bangalore, Karnataka, 560034, India.
Timothy L PruettDivision of Solid Organ Transplantation, Department of Surgery, University of Minnesota, Minneapolis, Minnesota, 55455, USA.
Joseph Sushil RaoDivision of Solid Organ Transplantation, Department of Surgery, University of Minnesota, Minneapolis, Minnesota, 55455, USA. jrao@umn.edu.ORCID https://orcid.org/0000-0002-0197-6107
Jeffrey TithofDepartment of Mechanical Engineering, University of Minnesota, 111 Church St SE, Minneapolis, Minnesota, 55455, USA. tithof@umn.edu.ORCID https://orcid.org/0000-0003-2083-0901

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This numerical study employs a computational model of human hepatic blood flow to investigate the hemodynamic consequences of cirrhosis. The liver receives blood through a dual-inlet system (portal vein and hepatic artery) that perfuses a complex network of sinusoids; however, cirrhosis-induced fibrosis distorts these channels, increasing hydraulic resistance. In turn, portal pressure is elevated, leading to the potential recanalization of portosystemic collaterals. We extended a lumped parameter hydraulic network model of the human liver, with demarcation of Couinaud segments, to capture the effects of fibrosis by incorporating a portosystemic collateral pathway and an "apparent viscosity" formulation that accounts for the non-Newtonian properties of blood. Our simulations indicate that segment-wise reductions in mean sinusoid conductance, combined with increased heterogeneity, drive the flow redistribution characteristic of the clinical "atrophy-hypertrophy complex". This results in diminished perfusion and wall shear stress in right-lobe segments, while flow and wall shear stress is preserved or even elevated in the left lobe. Sensitivity analysis suggests that the onset of portal hypertension is driven primarily by the reduction of mean sinusoid conductance, not increased heterogeneity. However, increased heterogeneity likely exacerbates liver dysfunction, as the model predicts that a disproportionately large fraction of blood passes through the relatively few sinusoids with the lowest hydraulic resistance. Additionally, results demonstrate that while the dilatation of portosystemic collaterals effectively offloads the portal system, it leads to a substantial increase in overall blood flow, contributing to hyperdynamic circulation (a hallmark feature of cirrhosis). These predictions provide quantitative, mechanistic insights into the hemodynamic and anatomical alterations of cirrhosis, offering a computational framework that helps explain clinical observations and may assist in future patient-specific surgical planning.

Indexed as

HemodynamicsLiverLiver CirrhosisModels, BiologicalComputer SimulationHumansLiver CirculationModels, CardiovascularStress, MechanicalCirrhosisComputational fluid dynamicsHepatic blood flowReduced order modeling

Identifiers

PMID42171825
PMCPMC13197283

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.