Evidence map›Paper›PMID 28303482›Full record

ArticleIntensive care medicine experimental2017

Extracellular superoxide dismutase is necessary to maintain renal blood flow during sepsis development.

Larissa Constantino, Letícia Selinger Galant, Francieli Vuolo, Karla Lorena Guarido, Luiza Wilges Kist, Giovanna Medeiros Tavares de Oliveira, Matheus Augusto de Bittencourt Pasquali, Cláudio Teodoro de Souza, José Eduardo da Silva-Santos, Maurício Reis Bogo and 3 more

Open access · goldAbstract read
In one paragraph

Article in Intensive care medicine experimental, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.2field-weighted citation impact, top 48% 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

12 citing papers in PubMed, 18 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

13 authors at 4 institutions in 1 country.

Larissa ConstantinoLaboratório de Fisiopatologia Experimental, Universidade do Extremo Sul Catarinense, Avenida Universitária, 1105, 88806-000, Criciúma, SC, Brazil.
Letícia Selinger GalantLaboratório de Fisiopatologia Experimental, Universidade do Extremo Sul Catarinense, Avenida Universitária, 1105, 88806-000, Criciúma, SC, Brazil.
Francieli VuoloLaboratório de Fisiopatologia Experimental, Universidade do Extremo Sul Catarinense, Avenida Universitária, 1105, 88806-000, Criciúma, SC, Brazil.
Karla Lorena GuaridoDepartamento de Farmacologia, Laboratório de Biologia Cardiovascular, Universidade Federal de Santa Catarina, Campus Trindade, CEP 88040-900, Florianópolis, SC, Brazil.
Luiza Wilges KistLaboratório de Biologia Genômica e Molecular, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul, Avenida Ipiranga, 6681, 90619-900, Porto Alegre, RS, Brazil.
Giovanna Medeiros Tavares de OliveiraLaboratório de Biologia Genômica e Molecular, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul, Avenida Ipiranga, 6681, 90619-900, Porto Alegre, RS, Brazil.
Matheus Augusto de Bittencourt PasqualiDepartamento de Bioquímica, Centro de Estudos em Estresse Oxidativo (Lab. 32), ICBS, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos, 2600-Anexo, CEP 90035-003, Porto Alegre, RS, Brazil.
Cláudio Teodoro de SouzaLaboratório de Fisiologia e Bioquímica do Exercício, Universidade do Extremo Sul Catarinense, Avenida Universitária, 1105, 88806-000, Criciúma, SC, Brazil.
José Eduardo da Silva-SantosDepartamento de Farmacologia, Laboratório de Biologia Cardiovascular, Universidade Federal de Santa Catarina, Campus Trindade, CEP 88040-900, Florianópolis, SC, Brazil.
Maurício Reis BogoLaboratório de Biologia Genômica e Molecular, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul, Avenida Ipiranga, 6681, 90619-900, Porto Alegre, RS, Brazil.
José Cláudio Fonseca MoreiraDepartamento de Bioquímica, Centro de Estudos em Estresse Oxidativo (Lab. 32), ICBS, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos, 2600-Anexo, CEP 90035-003, Porto Alegre, RS, Brazil.
Cristiane RitterLaboratório de Fisiopatologia Experimental, Universidade do Extremo Sul Catarinense, Avenida Universitária, 1105, 88806-000, Criciúma, SC, Brazil.
Felipe Dal-PizzolLaboratório de Fisiopatologia Experimental, Universidade do Extremo Sul Catarinense, Avenida Universitária, 1105, 88806-000, Criciúma, SC, Brazil. fdpizzol@gmail.com.
Universidade do Extremo Sul Catarinense · BRPontifícia Universidade Católica do Rio Grande do Sul · BRUniversidade Federal de Santa Catarina · BRUniversidade Federal do Rio Grande do Sul · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundExtracellular superoxide dismutase (ECSOD) protects nitric oxide (NO) bioavailability by decreasing superoxide levels and preventing peroxynitrite generation, which is important in maintaining renal blood flow and in preventing acute kidney injury. However, the profile of ECSOD expression after sepsis is not fully understood. Therefore, we intended to evaluate the content and gene expression of superoxide dismutase (SOD) isoforms in the renal artery and their relation to renal blood flow.

methodsSepsis was induced in Wistar rats by caecal ligation and perforation. Several times after sepsis induction, renal blood flow (12, 24 and 48 h); the renal arterial content of SOD isoforms, nitrotyrosine, endothelial and inducible nitric oxide synthase (e-NOS and i-NOS), and phosphorylated vasodilator-stimulated phosphoprotein (pVASP); and SOD activity (3, 6 and 12 h) were measured. The influence of a SOD inhibitor was also evaluated.

resultsAn increase in ECSOD content was associated with decreased 3-nitrotyrosine levels. These events were associated with an increase in pVASP content and maintenance of renal blood flow. Moreover, previous treatment with a SOD inhibitor increased nitrotyrosine content and reduced renal blood flow.

conclusionsECSOD appears to have a major role in decreasing peroxynitrite formation in the renal artery during the early stages of sepsis development, and its application can be important in renal blood flow control and maintenance during septic insult.

Indexed as

Acute renal failureNitric oxideSepsisSuperoxide

Identifiers

PMID28303482
PMCPMC5355399
OpenAlexW2596725502

What OpenQuestion holds

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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.