Evidence map›Paper›PMID 30919149›Full record

ArticleIntensive care medicine experimental2019

Exogenous surfactant prevents hyperoxia-induced lung injury in adult mice.

Frank Silva Bezerra, Camila de Oliveira Ramos, Thalles de Freitas Castro, Natália Pereira da Silva Araújo, Ana Beatriz Farias de Souza, Ana Carla Balthar Bandeira, Guilherme de Paula Costa, Christiane Teixeira Cartelle, André Talvani, Sílvia Dantas Cangussú and 2 more

Open access · goldAbstract read
In one paragraph

Article in Intensive care medicine experimental, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 29 citations in OpenAlex.

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  19. The Inhibitory Effect of CurosurfFrontiers in immunology · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Frank Silva BezerraLaboratory of Experimental Pathophysiology (LAFEx), Department of Biological Sciences (DECBI), Center of Research in Biological Sciences (NUPEB), Federal University of Ouro Preto (UFOP), Ouro Preto, Brazil. franksbezerra@hotmail.com.ORCID http://orcid.org/0000-0002-0804-5196
Camila de Oliveira RamosLaboratory of Experimental Pathophysiology (LAFEx), Department of Biological Sciences (DECBI), Center of Research in Biological Sciences (NUPEB), Federal University of Ouro Preto (UFOP), Ouro Preto, Brazil.
Thalles de Freitas CastroLaboratory of Experimental Pathophysiology (LAFEx), Department of Biological Sciences (DECBI), Center of Research in Biological Sciences (NUPEB), Federal University of Ouro Preto (UFOP), Ouro Preto, Brazil.
Natália Pereira da Silva AraújoLaboratory of Experimental Pathophysiology (LAFEx), Department of Biological Sciences (DECBI), Center of Research in Biological Sciences (NUPEB), Federal University of Ouro Preto (UFOP), Ouro Preto, Brazil.
Ana Beatriz Farias de SouzaLaboratory of Experimental Pathophysiology (LAFEx), Department of Biological Sciences (DECBI), Center of Research in Biological Sciences (NUPEB), Federal University of Ouro Preto (UFOP), Ouro Preto, Brazil.
Ana Carla Balthar BandeiraLaboratory of Experimental Pathophysiology (LAFEx), Department of Biological Sciences (DECBI), Center of Research in Biological Sciences (NUPEB), Federal University of Ouro Preto (UFOP), Ouro Preto, Brazil.
Guilherme de Paula CostaLaboratory of Immunobiology of Inflammation (LABIIN), Department of Biological Sciences (DECBI), Center of Research in Biological Sciences (NUPEB), Federal University of Ouro Preto (UFOP), Ouro Preto, Brazil.
Christiane Teixeira CartelleLaboratory of Neuro Immuno experimental pathology (NIPE), Department of Pathology, Institute of Biological Sciences, Federal University of Minas Gerais (UFMG), Belo Horizonte, Brazil.
André TalvaniLaboratory of Immunobiology of Inflammation (LABIIN), Department of Biological Sciences (DECBI), Center of Research in Biological Sciences (NUPEB), Federal University of Ouro Preto (UFOP), Ouro Preto, Brazil.
Sílvia Dantas CangussúLaboratory of Experimental Pathophysiology (LAFEx), Department of Biological Sciences (DECBI), Center of Research in Biological Sciences (NUPEB), Federal University of Ouro Preto (UFOP), Ouro Preto, Brazil.
Laurent BrochardKeenan Research Centre, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, ON, Canada.
Akinori Cardozo NagatoLaboratory of Immunopathology and Experimental Pathology, Center for Reproductive Biology-CRB, Federal University of Juiz de Fora, Juiz de Fora, Minas Gerais, Brazil.
Universidade Federal de Ouro Preto · BRSt. Michael's Hospital · CAUniversidade Federal de Juiz de Fora · BRUniversidade Federal de Minas Gerais · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn 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.

methodsMale 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.

resultsCompared 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.

conclusionOur 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.

Indexed as

ARDSBALB/c miceExogenous surfactantHyperoxiaLung injuryOxidative stress

Identifiers

PMID30919149
PMCPMC6437243
OpenAlexW2940505275

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.