Evidence map›Paper›PMID 12746231›Full record

ArticleBritish journal of pharmacology2003

Role of the bradykinin B2 receptor for the local and systemic inflammatory response that follows severe reperfusion injury.

Danielle G Souza, Vanessa Pinho, Jorge L Pesquero, Eliane S Lomez, Steve Poole, Luiz Juliano, Ary Correa, M Salete de A Castro, Mauro M Teixeira

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 49 citations in OpenAlex.

  1. Trial
  2. Trial
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  4. Article
  5. Synergistic Neuroprotection by a PAF Antagonist Plus a Docosanoid in Experimental Ischemic Stroke: Dose-Response and Therapeutic Window.Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association · 2022
    Article
  6. Article
  7. Kallistatin suppresses cancer development by multi-factorial actions.Critical reviews in oncology/hematology · 2017
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Bradykinin does not induce gap formation between human endothelial cells.Pflugers Archiv : European journal of physiology · 2008
    Article
  17. Article
  18. 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

9 authors at 2 institutions in 1 country.

Danielle G SouzaDepartamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Vanessa Pinho
Jorge L Pesquero
Eliane S Lomez
Steve Poole
Luiz Juliano
Ary Correa
M Salete de A Castro
Mauro M Teixeira
Universidade Federal de Minas Gerais · BRUniversidade Federal de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. Bradykinin (BK) appears to play an important role in the development and maintenance of inflammation. Here, we assessed the role of the BK B(2) receptor for the injuries that occur after ischemia and reperfusion (I/R) of the territory irrigated by the superior mesenteric artery. 2. Tissue (lung and duodenum) kallikrein activity increased after ischemia with greater enhancement after reperfusion. A selective inhibitor of tissue kallikrein, Phenylacetyl-Phe-Ser-Arg-N-(2,3-dinitrophenyl)-ethylenediamine (TKI, 0.001-10 mg ml(-1)), inhibited kallikrein activity in a concentration-dependent manner in vitro. In vivo, pretreatment with TKI (30 mg kg(-1)) prevented the extravasation of plasma and the recruitment of neutrophils. 3. Similarly, the bradykinin B(2) receptor antagonists, HOE 140 (0.01-1.0 mg kg(-1)) or FR173657 (10.0 mg kg(-1)), inhibited reperfusion-induced increases in vascular permeability and the recruitment of neutrophils in the intestine and lungs. 4. In a model of more severe I/R injury, HOE 140 (1.0 mg kg(-1)) inhibited the increase in vascular permeability, neutrophil recruitment, haemorrhage and tissue pathology. Furthermore, HOE 140 significantly inhibited the elevations of TNF-alpha in tissue and serum and partially prevented lethality. This was associated with an increase in the concentrations of IL-10 in tissue and serum. 5. Thus, our results demonstrate that, following intestinal I/R injury, there is an increase in tissue kallikrein activity and activation of BK B(2) receptors. B(2) receptor activation is essential for the development of inflammatory tissue injury and lethality. These results contrast with those of others showing that BK mostly exerts a protective role during I/R injury.

Indexed as

AnimalsBradykininBradykinin B2 Receptor AntagonistsCapillary PermeabilityDose-Response Relationship, DrugInflammationInterleukinsIntestinal MucosaIntestinesLungMaleMesenteric Artery, SuperiorNeutrophil InfiltrationOligopeptidesRatsRats, WistarBradykininBradykinin B2 Receptor AntagonistsicatibantInterleukinsOligopeptidesphenylacetyl-Phe-Ser-Arg-N-(2,4-dinitrophenyl)ethylenediamineReceptor, Bradykinin B2Tissue KallikreinsTumor Necrosis Factor-alpha

Identifiers

PMID12746231
PMCPMC1573815
OpenAlexW2032934648

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.