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Exogenous surfactant prevents hyperoxia-induced lung injury in adult mice

BACKGROUND: In addition to the risk of developing ventilator-induced lung injury, patients with ARDS are at risk of developing hyperoxic injury due the supra-physiological oxygen supplementation clinically required to reverse hypoxemia. Alterations of endogenous surfactant system participate in the...

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Detalles Bibliográficos
Autores principales: Bezerra, Frank Silva, Ramos, Camila de Oliveira, Castro, Thalles de Freitas, Araújo, Natália Pereira da Silva, de Souza, Ana Beatriz Farias, Bandeira, Ana Carla Balthar, Costa, Guilherme de Paula, Cartelle, Christiane Teixeira, Talvani, André, Cangussú, Sílvia Dantas, Brochard, Laurent, Nagato, Akinori Cardozo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer International Publishing 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6437243/
https://www.ncbi.nlm.nih.gov/pubmed/30919149
http://dx.doi.org/10.1186/s40635-019-0233-6
Descripción
Sumario:BACKGROUND: In addition to the risk of developing ventilator-induced lung injury, patients with ARDS are at risk of developing hyperoxic injury due the supra-physiological oxygen supplementation clinically required to reverse hypoxemia. Alterations of endogenous surfactant system participate in the pulmonary dysfunction observed in ARDS. Administration of exogenous surfactant could have protective effects during hyperoxia. METHODS: Male BALB/c mice (8–10 weeks), a strain highly sensitive to hyperoxia, received the exogenous surfactant-containing protein SP-B and SP-C by intranasal instillation 12 h before starting 24 h of exposure to hyperoxia in an inhalation chamber and were compared to mice receiving hyperoxia alone and to controls subjected to normoxia. RESULTS: Compared to the hyperoxia group, the administration of exogenous surfactant was able to reduce lung inflammation through a reduction in the influx of neutrophils and inflammatory biomarkers such as TNF, IL-17, and HMGB1 expression. The antioxidant activity prevented oxidative damage by reducing lipid peroxidation and protein carbonylation and increasing superoxide dismutase activity when compared to the hyperoxia group. CONCLUSION: Our results offer new perspectives on the effects and the mechanism of exogenous surfactant in protecting the airway and lungs, in oxygen-rich lung microenvironment, against oxidative damage and aggravation of acute inflammation induced by hyperoxia.