ArticleAmerican journal of physiology. Lung cellular and molecular physiology2025
Dynamic driving pressure predicts ventilator-induced lung injury in mice with and without endotoxin-induced acute lung injury.
Article in American journal of physiology. Lung cellular and molecular physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Heliox ventilation promotes pulmonary circulation and cardiac function in elderly hypertensive patients: a randomized controlled trial.Medical gas research · 2026Trial
- Low PEEP ventilation in TGF-β1 induced lung injury triggers a reversible lung mechanical deterioration without promoting persistent structural damage.Scientific reports · 2026Article
- Revisiting ventilator-induced lung injury: from mechanical power to immunometabolic interaction.Frontiers in immunology · 2026Review
- Computer model-based injury prediction and evaluation of lung function in mice with acute and ventilator-induced lung injuries.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Application of neurally adjusted ventilatory assist (NAVA): a narrative review.Journal of thoracic disease · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Mechanical ventilation (MV) is a necessary lifesaving intervention for patients with acute respiratory distress syndrome (ARDS) but it can cause ventilator-induced lung injury (VILI), which contributes to the high ARDS mortality rate (∼40%). Bedside determination of optimally lung-protective ventilation settings is challenging because the evolution of VILI is not immediately reflected in clinically available, patient-level, data. The goal of this work was therefore to test ventilation waveform-derived parameters that represent the degree of ongoing VILI and can serve as targets for ventilator adjustments. VILI was generated at three different positive end-expiratory pressures in a murine inflammation-mediated (lipopolysaccharide, LPS) acute lung injury model and in initially healthy controls. LPS injury increased the expression of proinflammatory cytokines and caused widespread atelectasis, predisposing the lungs to VILI as measured in structure, mechanical function, and inflammation. Changes in lung function were used as response variables in an elastic net regression model that predicted VILI severity from tidal volume, dynamic driving pressure (PD
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