Evidence map›Paper›PMID 19630831›Full record

ReviewBritish journal of pharmacology2009

Role of nitroso radicals as drug targets in circulatory shock.

Emanuela Esposito, Salvatore Cuzzocrea

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

8 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Endothelium in pharmacology: 30 years on.British journal of pharmacology · 2009
    Article
  8. Article
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

2 authors at 2 institutions in 1 country.

Emanuela EspositoIRCCS Centro Neurolesi Bonino-Pulejo, Messina, Italy.
Salvatore Cuzzocrea
Istituti di Ricovero e Cura a Carattere Scientifico · ITUniversity of Messina · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A vast amount of circumstantial evidence implicates oxygen-derived free radicals (especially, superoxide and hydroxyl radical) and high-energy oxidants [such as peroxynitrite (OONO(-))] as mediators of shock and ischaemia/reperfusion injury. Reactive oxygen species can initiate a wide range of toxic oxidative reactions. These include initiation of lipid peroxidation, direct inhibition of mitochondrial respiratory chain enzymes, inactivation of glyceraldehyde-3 phosphate dehydrogenase, inhibition of membrane sodium/potassium adenosine 5'-triphosphate-ase activity, inactivation of membrane sodium channels and other oxidative modifications of proteins. All these toxicities are likely to play a role in the pathophysiology of shock and ischaemia and reperfusion. Moreover, various studies have clearly shown that treatment with either OONO(-) decomposition catalysts, which selectively inhibit OONO(-), or with superoxide dismutase (SOD) mimetics, which selectively mimic the catalytic activity of the human SOD enzymes, have been shown to prevent in vivo the delayed vascular decompensation and the cellular energetic failure associated with shock and ischaemia/reperfusion injury.

Indexed as

Drug Delivery SystemsAnimalsAntioxidantsHumansMetalloporphyrinsModels, BiologicalMolecular StructureReactive Nitrogen SpeciesReactive Oxygen SpeciesReperfusion InjuryShock, CardiogenicSuperoxide DismutaseAntioxidantsMetalloporphyrinsReactive Nitrogen SpeciesReactive Oxygen SpeciesSuperoxide Dismutase

Identifiers

PMID19630831
PMCPMC2707962
OpenAlexW1496919424

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.