High-tidal-volume ventilation increases lung fibrosis in acute lung injury
Author Information
Author(s): Li Li-Fu, Liao Shuen-Kuei, Huang Chung-Chi, Hung Ming-Jui, Quinn Deborah A
Primary Institution: Chang Gung Memorial Hospital
Hypothesis
High-tidal-volume ventilation increases pulmonary fibrosis in acute lung injury via the Akt and MAPK pathways.
Conclusion
High-tidal-volume ventilation-induced lung fibrosis was dependent on the activation of the Akt and ERK1/2 pathways.
Supporting Evidence
- High-tidal-volume ventilation increased type I and type III procollagen mRNA expression.
- Microvascular permeability and hydroxyproline content were elevated in the high-tidal-volume group.
- Pharmacologic inhibition of ERK1/2 reduced lung fibrosis.
- High-tidal-volume ventilation increased MIP-2 production but decreased IP-10 production.
Takeaway
Using a mouse model, researchers found that using high amounts of air during ventilation can make lung scarring worse after injury, and this happens because of certain pathways in the body.
Methodology
Male C57BL/6 mice were treated with bleomycin to induce acute lung injury and then subjected to either high-tidal-volume or low-tidal-volume mechanical ventilation.
Limitations
The study was conducted in a mouse model, which may not fully replicate human responses.
Participant Demographics
Male C57BL/6 mice, aged 6-8 weeks, weighing 20-25 g.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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