Evidence map›Paper›PMID 20423344›Full record

ArticleBritish journal of pharmacology2010

Ouabain attenuates cardiotoxicity induced by other cardiac steroids.

M Nesher, U Shpolansky, N Viola, M Dvela, N Buzaglo, H Cohen Ben-Ami, H Rosen, D Lichtstein

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2010. 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
1.1field-weighted citation impact, top 25% 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, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Sensational site: the sodium pump ouabain-binding site and its ligands.American journal of physiology. Cell physiology · 2024
    Review
  4. Article
  5. Synthesis and Biological Evaluation of Novel Bufalin Derivatives.International journal of molecular sciences · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Na⁺Molecules (Basel, Switzerland) · 2017
    Review
  14. Endogenous Ouabain: Recent Advances and Controversies.Hypertension (Dallas, Tex. : 1979) · 2016
    Review
  15. Review
  16. Review
  17. Article
  18. Rethinking Heart Failure.Cardiology research · 2012
    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

8 authors at 1 institution in 1 country.

M NesherDepartment of Medical Neurobiology, Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah Medical School, Jerusalem, Israel.
U Shpolansky
N Viola
M Dvela
N Buzaglo
H Cohen Ben-Ami
H Rosen
D Lichtstein
Essex Cardiothoracic Centre · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeAll cardiac steroids have a similar structure, bind to and inhibit the ubiquitous transmembrane protein Na(+), K(+)-ATPase and increase the force of contraction of heart muscle. However, there are diverse biological responses to different cardiac steroids both at the cellular and at the molecular level. Moreover, we have recently shown that ouabain inhibits digoxin- and bufalin-induced changes in membrane traffic. The present study was designed to test the hypothesis that ouabain also has an inhibitory effect on cardiotoxicity induced by other cardiac steroids. EXPERIMENTAL APPROACH: The hypothesis was tested in isolated heart muscle preparations and in an in vivo model of cardiotoxicity in guinea pigs. KEY

resultsOuabain at a low dose attenuated the toxicity induced by bufalin and digoxin in heart muscle preparations. In addition, ouabain at the low dose (91 ng.kg(-1).h(-1)), but not at a higher dose (182 ng.kg(-1).h(-1)), delayed the development of digoxin-induced (500 microg.kg(-1).h(-1)) cardiotoxicity in anaesthetized guinea pigs, as manifested by delayed arrhythmia and terminal ventricular fibrillation, as well as a reduced heart rate. In addition, as observed with ouabain, the phosphoinositide 3-kinase inhibitor wortmannin (100 microg.kg(-1).h(-1)) delayed the digoxin-induced arrhythmia in anaesthetized guinea pigs. CONCLUSIONS AND IMPLICATIONS: The present study demonstrates the inhibitory effect, probably through signal transduction pathways, of ouabain on digoxin- and bufalin-induced cardiotoxicity in guinea pigs. Further understanding of this phenomenon could be beneficial for increasing the therapeutic window for cardiac steroids in the treatment of chronic heart failure.

Indexed as

AndrostadienesAnimalsArrhythmias, CardiacBufanolidesCardiotonic AgentsDigoxinDose-Response Relationship, DrugGuinea PigsHeart RateMaleMyocardiumOuabainPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsSignal TransductionSodium-Potassium-Exchanging ATPaseAndrostadienesbufalinBufanolidesCardiotonic AgentsDigoxinOuabainPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsSodium-Potassium-Exchanging ATPaseWortmannin

Identifiers

PMID20423344
PMCPMC2874856
OpenAlexW1749996095

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.