Evidence map›Paper›PMID 20453164›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2010

Nitric oxide synthase 3 contributes to ventilator-induced lung injury.

Katerina Vaporidi, Roland C Francis, Kenneth D Bloch, Warren M Zapol

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 43 citations in OpenAlex.

  1. Trial
  2. Review
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  4. Article
  5. Glycyl-L-histidyl-L-lysine-CuFrontiers in molecular biosciences · 2022
    Article
  6. Review
  7. Article
  8. Hypoxia treatment reverses neurodegenerative disease in a mouse model of Leigh syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Hemoglobin infusion does not alter murine pulmonary vascular tone.Nitric oxide : biology and chemistry · 2013
    Article
  16. Article
  17. Article
  18. Pulmonary microRNA profiling in a mouse model of ventilator-induced lung injury.American journal of physiology. Lung cellular and molecular physiology · 2012
    Article
  19. Activation of calpains mediates early lung neutrophilic inflammation in ventilator-induced lung injury.American journal of physiology. Lung cellular and molecular physiology · 2012
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Katerina VaporidiAnesthesia Center for Critical Care Research, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA.
Roland C Francis
Kenneth D Bloch
Warren M Zapol
Harvard University · USMassachusetts General Hospital · US

Funding

BMPR2 and the Pathogenesis of Pulmonary HypertensionR01HL074352 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI BLOCH, KENNETH D · 2003 to 2011
$3.7M
INHALED NITRIC OXIDER01HL042397 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI ZAPOL, WARREN MYRON · 1990 to 2007
$2.8M
NHLBI NIH HHS HL-42397NHLBI NIH HHS R01 HL074352
6 · The paper itself

Abstract

Nitric oxide synthase (NOS) depletion or inhibition reduces ventilator-induced lung injury (VILI), but the responsible mechanisms remain incompletely defined. The aim of this study was to elucidate the role of endothelial NOS, NOS3, in the pathogenesis of VILI in an in vivo mouse model. Wild-type and NOS3-deficient mice were ventilated with high-tidal volume (HV(T); 40 ml/kg) for 4 h, with and without adding NO to the inhaled gas. Additional wild-type mice were pretreated with tetrahydrobiopterin and ascorbic acid, agents that can prevent NOS-generated superoxide production. Arterial blood gas tensions, histology, and lung mechanics were evaluated after 4 h of HV(T) ventilation. The concentration of protein, IgM, cytokines, malondialdehyde, and 8-isoprostane were measured in bronchoalveolar lavage fluid (BALF). Myeloperoxidase activity, total and oxidized glutathione levels, and NOS-derived superoxide production were measured in lung tissue homogenates. HV(T) ventilation induced VILI in wild-type mice, as reflected by decreased lung compliance, increased concentrations of protein and cytokines in BALF, and oxidative stress. All indices of VILI were ameliorated in NOS3-deficient mice. Augmenting pulmonary NO levels by breathing NO during mechanical ventilation did not increase lung injury in NOS3-deficient mice. HV(T) ventilation increased NOS-inhibitable superoxide production in lung extracts from wild-type mice but not in those from NOS3-deficient mice. Administration of tetrahydrobiopterin and ascorbic acid ameliorated VILI in wild-type mice. Our results indicate that NOS3 contributes to ventilator-induced lung injury via increased production of superoxide.

Indexed as

AnimalsAscorbic AcidBiopterinsBronchoalveolar Lavage FluidCytokinesDisease Models, AnimalImmunoglobulin MMaleMiceMice, Inbred C57BLNitric OxideNitric Oxide Synthase Type IIIOxidative StressSuperoxidesVentilator-Induced Lung InjuryAscorbic AcidBiopterinsCytokinesImmunoglobulin MNitric OxideNitric Oxide Synthase Type IIINos3 protein, mousesapropterinSuperoxides

Identifiers

PMID20453164
PMCPMC2928605
OpenAlexW2053061521

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.