Evidence map›Paper›PMID 35869495›Full record

ArticleLaboratory animal research2022

Ventilator-induced lung injury results in oxidative stress response and mitochondrial swelling in a mouse model.

Jon Petur Joelsson, Arni Asbjarnarson, Snaevar Sigurdsson, Jennifer Kricker, Bryndis Valdimarsdottir, Holmfridur Thorarinsdottir, Eir Starradottir, Thorarinn Gudjonsson, Saevar Ingthorsson, Sigurbergur Karason

Open access · diamondAbstract read
In one paragraph

Article in Laboratory animal research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

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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

10 authors at 2 institutions in 2 countries.

Jon Petur JoelssonUniversity of Iceland, Reykjavík, Iceland. jpj@hi.is.ORCID http://orcid.org/0000-0002-3261-4504
Arni AsbjarnarsonUniversity of Iceland, Reykjavík, Iceland.
Snaevar SigurdssonUniversity of Iceland, Reykjavík, Iceland.
Jennifer KrickerUniversity of Iceland, Reykjavík, Iceland.
Bryndis ValdimarsdottirUniversity of Iceland, Reykjavík, Iceland.
Holmfridur ThorarinsdottirUniversity of Iceland, Reykjavík, Iceland.
Eir StarradottirLandspitali University Hospital, Reykjavik, Iceland.
Thorarinn GudjonssonUniversity of Iceland, Reykjavík, Iceland.
Saevar IngthorssonUniversity of Iceland, Reykjavík, Iceland.
Sigurbergur KarasonUniversity of Iceland, Reykjavík, Iceland.
University of Iceland · ISReykjavík University · IS

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMechanical ventilation is a life-saving therapy for critically ill patients, providing rest to the respiratory muscles and facilitating gas exchange in the lungs. Ventilator-induced lung injury (VILI) is an unfortunate side effect of mechanical ventilation that may lead to serious consequences for the patient and increase mortality. The four main injury mechanisms associated with VILI are: baro/volutrauma caused by overstretching the lung tissues; atelectrauma, caused by repeated opening and closing of the alveoli resulting in shear stress; oxygen toxicity due to use of high ratio of oxygen in inspired air, causing formation of free radicals; and biotrauma, the resulting biological response to tissue injury, that leads to a cascade of events due to excessive inflammatory reactions and may cause multi-organ failure. An often-overlooked part of the inflammatory reaction is oxidative stress. In this research, a mouse model of VILI was set up with three tidal volume settings (10, 20 and 30 mL/kg) at atmospheric oxygen level. Airway pressures and heart rate were monitored and bronchoalveolar lavage fluid (BALF) and lung tissue samples were taken.

resultsWe show a correlation between increased inflammation and barrier failure, and higher tidal volumes, evidenced by increased IL-6 expression, high concentration of proteins in BALF along with changes in expression of adhesion molecules. Furthermore, swelling of mitochondria in alveolar type II cells was seen indicating their dysfunction and senescence-like state. RNA sequencing data present clear increases in inflammation, mitochondrial biogenesis and oxidative stress as tidal volume is increased, supported by degradation of Keap1, a redox-regulated substrate adaptor protein.

conclusionsOxidative stress seems to be a more prominent mechanism of VILI than previously considered, indicating that possible treatment methods against VILI might be identified by impeding oxidative pathways.

Indexed as

Acute lung injuryMouse studiesOxidative stressVentilator-induced lung injury

Identifiers

PMID35869495
PMCPMC9308307
OpenAlexW4286561088

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LicenceCC BY
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Registered trials

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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.