Evidence map›Paper›PMID 20602787›Full record

ArticleCritical care (London, England)2010

Time course of nitric oxide synthases, nitrosative stress, and poly(ADP ribosylation) in an ovine sepsis model.

Matthias Lange, Rhykka Connelly, Daniel L Traber, Atsumori Hamahata, Yoshimitsu Nakano, Aimalohi Esechie, Collette Jonkam, Sanna von Borzyskowski, Lillian D Traber, Frank C Schmalstieg and 2 more

Open access · goldAbstract read
In one paragraph

Article in Critical care (London, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.6field-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

26 citing papers in PubMed, 45 citations in OpenAlex.

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  11. OXIDATIVE STRESS IN A RAT MODEL OF COTTON SMOKE INHALATION-INDUCED PULMONARY INJURY.African journal of traditional, complementary, and alternative medicines : AJTCAM · 2016
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  20. Selective V(1a) agonism attenuates vascular dysfunction and fluid accumulation in ovine severe sepsis.American journal of physiology. Heart and circulatory physiology · 2012
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 1 institution in 2 countries.

Matthias LangeDepartment of Anesthesiology, Investigational Intensive Care Unit, The University of Texas Medical Branch and Shriners Burns Hospital for Children, 301 University Boulevard, Galveston, Texas 77550, USA. lanm@gmx.de
Rhykka Connelly
Daniel L Traber
Atsumori Hamahata
Yoshimitsu Nakano
Aimalohi Esechie
Collette Jonkam
Sanna von Borzyskowski
Lillian D Traber
Frank C Schmalstieg
David N Herndon
Perenlei Enkhbaatar
Shriners Hospitals for Children - Galveston · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionDifferent isoforms of nitric oxide synthases (NOS) and determinants of oxidative/nitrosative stress play important roles in the pathophysiology of pulmonary dysfunction induced by acute lung injury (ALI) and sepsis. However, the time changes of these pathogenic factors are largely undetermined.

methodsTwenty-four chronically instrumented sheep were subjected to inhalation of 48 breaths of cotton smoke and instillation of live Pseudomonas aeruginosa into both lungs and were euthanized at 4, 8, 12, 18, and 24 hours post-injury. Additional sheep received sham injury and were euthanized after 24 hrs (control). All animals were mechanically ventilated and fluid resuscitated. Lung tissue was obtained at the respective time points for the measurement of neuronal, endothelial, and inducible NOS (nNOS, eNOS, iNOS) mRNA and their protein expression, calcium-dependent and -independent NOS activity, 3-nitrotyrosine (3-NT), and poly(ADP-ribose) (PAR) protein expression.

resultsThe injury induced severe pulmonary dysfunction as indicated by a progressive decline in oxygenation index and concomitant increase in pulmonary shunt fraction. These changes were associated with an early and transient increase in eNOS and an early and profound increase in iNOS expression, while expression of nNOS remained unchanged. Both 3-NT, a marker of protein nitration, and PAR, an indicator of DNA damage, increased early but only transiently.

conclusionsIdentification of the time course of the described pathogenetic factors provides important additional information on the pulmonary response to ALI and sepsis in the ovine model. This information may be crucial for future studies, especially when considering the timing of novel treatment strategies including selective inhibition of NOS isoforms, modulation of peroxynitrite, and PARP.

Indexed as

Acute Lung InjuryAnimalsDisease Models, AnimalInterleukin-8LungNitratesNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINitritesPoly Adenosine Diphosphate RiboseReverse Transcriptase Polymerase Chain ReactionSepsisSheepTime FactorsTyrosine3-nitrotyrosineInterleukin-8NitratesNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINitritesPoly Adenosine Diphosphate RiboseTyrosine

Identifiers

PMID20602787
PMCPMC2945093
OpenAlexW2148183457

What OpenQuestion holds

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LicenceCC BY
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.