Evidence map›Paper›PMID 25516652›Full record

ArticleWorld journal of gastroenterology2014

Hepatoprotective effect of nitric oxide in experimental model of acute hepatic failure.

Marek Saracyn, Marek Brytan, Robert Zdanowski, Tomasz Ząbkowski, Przemysław Dyrla, Janusz Patera, Stanisław Wojtuń, Wojciech Kozłowski, Zofia Wańkowicz

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 42% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Review
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

9 authors at 1 institution in 1 country.

Marek SaracynMarek Saracyn, Zofia Wańkowicz, Department of Internal Diseases, Nephrology and Dialysis, Military Institute of Medicine, 04-141 Warsaw, Poland.
Marek BrytanMarek Saracyn, Zofia Wańkowicz, Department of Internal Diseases, Nephrology and Dialysis, Military Institute of Medicine, 04-141 Warsaw, Poland.
Robert ZdanowskiMarek Saracyn, Zofia Wańkowicz, Department of Internal Diseases, Nephrology and Dialysis, Military Institute of Medicine, 04-141 Warsaw, Poland.
Tomasz ZąbkowskiMarek Saracyn, Zofia Wańkowicz, Department of Internal Diseases, Nephrology and Dialysis, Military Institute of Medicine, 04-141 Warsaw, Poland.
Przemysław DyrlaMarek Saracyn, Zofia Wańkowicz, Department of Internal Diseases, Nephrology and Dialysis, Military Institute of Medicine, 04-141 Warsaw, Poland.
Janusz PateraMarek Saracyn, Zofia Wańkowicz, Department of Internal Diseases, Nephrology and Dialysis, Military Institute of Medicine, 04-141 Warsaw, Poland.
Stanisław WojtuńMarek Saracyn, Zofia Wańkowicz, Department of Internal Diseases, Nephrology and Dialysis, Military Institute of Medicine, 04-141 Warsaw, Poland.
Wojciech KozłowskiMarek Saracyn, Zofia Wańkowicz, Department of Internal Diseases, Nephrology and Dialysis, Military Institute of Medicine, 04-141 Warsaw, Poland.
Zofia WańkowiczMarek Saracyn, Zofia Wańkowicz, Department of Internal Diseases, Nephrology and Dialysis, Military Institute of Medicine, 04-141 Warsaw, Poland.
National Academy of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo evaluate the effect of nitric oxide (NO) on the development and degree of liver failure in an animal model of acute hepatic failure (AHF).

methodsAn experimental rat model of galactosamine-induced AHF was used. An inhibitor of NO synthase, nitroarginine methyl ester, or an NO donor, arginine, were administered at various doses prior to or after the induction of AHF.

resultsAll tested groups developed AHF. Following inhibition of the endogenous NO pathway, most liver parameters improved, regardless of the inhibitor dose before the induction of liver damage, and depending on the inhibitor dose after liver damage. Prophylactic administration of the inhibitor was more effective in improving liver function parameters than administration of the inhibitor after liver damage. An attempt to activate the endogenous NO pathway prior to the induction of liver damage did not change the observed liver function parameters. Stimulation of the endogenous NO pathway after liver damage, regardless of the NO donor dose used, improved most liver function parameters.

conclusionThe endogenous NO pathway plays an important role in the development of experimental galactosamine-induced AHF.

Indexed as

AnimalsBiomarkersChemical and Drug Induced Liver InjuryCytoprotectionDisease Models, AnimalEnzyme InhibitorsGalactosamineLiverLiver Failure, AcuteMaleNitric OxideNitric Oxide DonorsNitric Oxide SynthaseRats, Sprague-DawleySignal TransductionTime FactorsBiomarkersEnzyme InhibitorsGalactosamineNitric OxideNitric Oxide DonorsNitric Oxide SynthaseAcute hepatic failureGalactosamineNitric oxideNitric oxide synthaseRat model

Identifiers

PMID25516652
PMCPMC4265599
OpenAlexW1964011854

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.