ArticleCritical care research and practice2011
Plasminogen activator inhibitor-type I gene deficient mice show reduced influx of neutrophils in ventilator-induced lung injury.
Article in Critical care research and practice, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
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Who cites it
7 citing papers in PubMed.
- D-Dimer: A Mediator of the Association Between Lymphocyte and Dissemination of Pulmonary Tuberculosis: A Retrospective Cohort Study.The clinical respiratory journal · 2026Article
- Ventilator-Induced Lung Injury: Mechanotransduction and Potential Therapeutic Targets.MedComm · 2026Review
- Mining the key genes for ventilator-induced lung injury using co-expression network analysis.Bioscience reports · 2021Article
- Plasma Cold-Inducible RNA-Binding Protein Predicts Lung Dysfunction After Cardiovascular Surgery Following Cardiopulmonary Bypass: A Prospective Observational Study.Medical science monitor : international medical journal of experimental and clinical research · 2019Observational
- Effects of Zinc Finger Protein A20 on Lipopolysaccharide (LPS)-Induced Pulmonary Inflammation/Anti-Inflammatory Mediators in an Acute Lung Injury/Acute Respiratory Distress Syndrome Rat Model.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- Plasminogen activator inhibitor-1 does not contribute to the pulmonary pathology induced by acute exposure to ozone.Physiological reports · 2016Article
- In vivo evidence for an endothelium-dependent mechanism in radiation-induced normal tissue injury.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ventilator-induced lung injury (VILI) is associated with inhibition of the fibrinolytic system secondary to increased production of plasminogen activator inhibitor- (PAI-)1. To determine the role of PAI-1 on pulmonary coagulopathy and inflammation during mechanical ventilation, PAI-1 gene-deficient mice and their wild-type littermates were anesthetized (control), or anesthetized, tracheotomized and subsequently ventilated for 5 hours with either low tidal volumes (LV(T)) or high tidal volumes (HV(T)). VILI was assessed by pulmonary coagulopathy, lung wet-to-dry ratios, total protein level in bronchoalveolar lavage fluid, neutrophil influx, histopathology, and pulmonary and plasma cytokine levels. Ventilation resulted in pulmonary coagulopathy and inflammation, with more injury following ventilation with HV(T) as compared to LV(T). In PAI-1 gene-deficient mice, the influx of neutrophils in the pulmonary compartment was attenuated, while increased levels of pulmonary cytokines were found. Other endpoints of VILI were not different between PAI-1 gene-deficient and wild-type mice. These data indicate that a defect fibrinolytic response attenuates recruitment of neutrophils in VILI.
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Registered trials
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