Evidence map›Paper›PMID 26895462›Full record

ArticleBritish journal of pharmacology2016

Therapeutic time window for angiotensin-(1-7) in acute lung injury.

Stefanie Supé, Franziska Kohse, Florian Gembardt, Wolfgang M Kuebler, Thomas Walther

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. The Race for ACE: Targeting Angiotensin-Converting Enzymes (ACE) in SARS-CoV-2 Infection.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2022
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. COVID-19 and cardiovascular diseases.Journal of cardiology · 2020
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Lipoxin AInnate immunity · 2018
    Article
  17. Article
  18. Article
  19. Angiotensin-(1-7) inhibits inflammation and oxidative stress to relieve lung injury induced by chronic intermittent hypoxia in rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2016
    Article
  20. 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

5 authors at 4 institutions in 3 countries.

Stefanie SupéInstitute of Physiology, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Franziska KohseInstitute of Physiology, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Florian GembardtDepartment of Cardiac Pathobiology, Excellence Cluster Cardiopulmonary System, Gießen, Germany.
Wolfgang M KueblerInstitute of Physiology, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Thomas WaltherDepartment of Pharmacology and Therapeutics, University College Cork, Cork, Ireland.
Charité - Universitätsmedizin Berlin · DECardio-Pulmonary Institute · DEUniversity Hospital Leipzig · DEUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeThere is presently no proven pharmacological therapy for the acute respiratory distress syndrome. Recently, we and others discovered that the heptapeptide angiotensin-(1-7) [Ang-(1-7)] shows significant beneficial effects in preclinical models of acute lung injury (ALI). Here, we aimed to identify the best time window for Ang-(1-7) administration to protect rats from oleic acid (OA) induced ALI. EXPERIMENTAL APPROACH: The effects of i.v. infused Ang-(1-7) were examined over four different time windows before or after induction of ALI in male Sprague-Dawley rats. Haemodynamic effects were continuously monitored, and loss of barrier function, inflammation and lung peptidase activities were measured as experimental endpoints. KEY

resultsAng-(1-7) infusion provided the best protection against experimental ALI when administered by continuous infusion starting immediately after 30 min OA infusion till the end of the experiment (30-240 min). Both pretreatment (-60 to 0 min before OA) and short-term therapy (30-90 min) also had beneficial effects although less pronounced than the effects achieved with the optimal therapy window. Starting infusion of Ang-(1-7) 60 min after the end of OA treatment (90-240 min) did not protect barrier function or haemodynamics but still reduced myeloperoxidase activity and increased ACE2/ACE activity ratio respectively. CONCLUSIONS AND IMPLICATIONS: Our findings indicate that early initiation of therapy after ALI and continuous drug delivery are most beneficial for optimal therapeutic efficiency of Ang-(1-7) treatment in experimental ALI and, presumably accordingly, in clinical acute respiratory distress syndrome.

Indexed as

Acute Lung InjuryAngiotensin IAnimalsHemodynamicsInfusions, IntravenousMaleOleic AcidPeptide FragmentsRatsRats, Sprague-DawleyTime FactorsAngiotensin Iangiotensin I (1-7)Oleic AcidPeptide Fragments

Identifiers

PMID26895462
PMCPMC4842919
OpenAlexW2283365023

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.