ArticleIntensive care medicine experimental2024
Regional distribution of mechanical strain and macrophage-associated lung inflammation after ventilator-induced lung injury: an experimental study.
Article in Intensive care medicine experimental, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Quantitative assessment of lung mechanical properties in ARDS using X-ray computed tomography.Intensive care medicine experimental · 2026Review
- Macrophage-specific therapy blocks the lung's mechanosensitive immune response to alveolar distension.JCI insight · 2025Article
- Imaging in animal models: bridging experimental findings and human pathophysiology.Critical care (London, England) · 2025Review
- Novel lung imaging techniques: new experimental insights in acute respiratory failure.Intensive care medicine experimental · 2025Article
- Macrophage-specific lipid nanoparticle therapy blocks the lung's mechanosensitive immunity due to macrophage-epithelial interactions.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
backgroundAlveolar macrophages activation to the pro-inflammatory phenotype M1 is pivotal in the pathophysiology of Ventilator-Induced Lung Injury (VILI). Increased lung strain is a known determinant of VILI, but a direct correspondence between regional lung strain and macrophagic activation remains unestablished. [
methodsSeven anesthetized pigs underwent VILI, while three served as control. Lung CT scans were acquired at incremental tidal volumes, simultaneously recording lung mechanics. [
resultsCompared to controls, the VILI group exhibited statistically significant higher VoStrain and Standardized Uptake Value Ratios (SUVR) both at Para-D and Mid-T levels. Both VoStrain and SUVR increased along the gravitational axis with an increment described by statistically different regression lines between VILI and healthy controls and reaching the peak in the dependent regions of the lung (for strain in VILI vs. control was at Para-D: 760 ± 210 vs. 449 ± 106; at Mid-T level 497 ± 373 vs. 193 ± 160; for SUVR, in VILI vs. control was at Para-D: 2.2 ± 1.3 vs. 1.3 ± 0.1; at Mid-T level 1.3 ± 1.0 vs. 0.6 ± 0.03). LMI in both Para-D and Mid-T was statistically significantly higher in VILI than in controls.
conclusionsIn this porcine model of VILI, we found a topographical correlation between lung strain and [
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Registered trials
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