Evidence map›Paper›PMID 24412579›Full record

ArticleJournal of molecular and cellular cardiology2014

Reduced Na⁺ current density underlies impaired propagation in the diabetic rabbit ventricle.

Catherine L Stables, Hassan Musa, Aditi Mitra, Sandesh Bhushal, Makarand Deo, Guadalupe Guerrero-Serna, Sergey Mironov, Manuel Zarzoso, Karen L Vikstrom, William Cawthorn and 1 more

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-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

23 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Observational
  5. Dysglycemia and arrhythmias.World journal of diabetes · 2023
    Review
  6. Article
  7. Article
  8. CaPflugers Archiv : European journal of physiology · 2022
    Review
  9. Review
  10. Article
  11. Review
  12. Electrocardiological effects of ranolazine and lidocaine on normal and diabetic rat atrium.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2021
    Article
  13. Review
  14. Review
  15. Loss of insulin signaling may contribute to atrial fibrillation and atrial electrical remodeling in type 1 diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  16. Article
  17. Article
  18. Disease Modifiers of InheritedFrontiers in cardiovascular medicine · 2018
    Review
  19. Review
  20. 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

11 authors at 2 institutions in 1 country.

Catherine L StablesCenter for Arrhythmia Research, Department of Internal Medicine-Cardiology, University of Michigan, Ann Arbor, MI, USA.
Hassan MusaCenter for Arrhythmia Research, Department of Internal Medicine-Cardiology, University of Michigan, Ann Arbor, MI, USA.
Aditi MitraCenter for Arrhythmia Research, Department of Internal Medicine-Cardiology, University of Michigan, Ann Arbor, MI, USA.
Sandesh BhushalDepartment of Engineering, Norfolk State University, Norfolk, VA, USA.
Makarand DeoDepartment of Engineering, Norfolk State University, Norfolk, VA, USA.
Guadalupe Guerrero-SernaCenter for Arrhythmia Research, Department of Internal Medicine-Cardiology, University of Michigan, Ann Arbor, MI, USA.
Sergey MironovCenter for Arrhythmia Research, Department of Internal Medicine-Cardiology, University of Michigan, Ann Arbor, MI, USA.
Manuel ZarzosoCenter for Arrhythmia Research, Department of Internal Medicine-Cardiology, University of Michigan, Ann Arbor, MI, USA.
Karen L VikstromCenter for Arrhythmia Research, Department of Internal Medicine-Cardiology, University of Michigan, Ann Arbor, MI, USA.
William CawthornDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.
Sandeep V PanditCenter for Arrhythmia Research, Department of Internal Medicine-Cardiology, University of Michigan, Ann Arbor, MI, USA. Electronic address: sanpandi@med.umich.edu.
University of Michigan–Ann Arbor · USNorfolk State University · US

Funding

PUBLIC HEALTH DEMONSTRATIONP60DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MYERS, MARTIN G · 1985 to 2012
$26.5M
Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
THREE DIMENSIONAL VORTEX LIKE REENTRY IN CORONARY PERFUSED VENTRICULAR WALLP01HL039707 · NHLBI · UPSTATE MEDICAL UNIVERSITY · PI ZAITSEV, ALEXEY V · 1990 to 2010
$19.0M
P3: Biophysical Mechanisms in two Arhythmogenic DiseasesP01HL087226 · NHLBI · UPSTATE MEDICAL UNIVERSITY · PI JALIFE, JOSE S · 2007 to 2012
$10.3M
NHLBI NIH HHS P01 HL039707NHLBI NIH HHS P01HL039707NHLBI NIH HHS P01 HL087226NHLBI NIH HHS P01HL087226NIDDK NIH HHS 5P60 DK20572NIDDK NIH HHS P30 DK020572NIDDK NIH HHS P60 DK020572
6 · The paper itself

Abstract

Diabetes is associated with an increased risk of sudden cardiac death, but the underlying mechanisms remain unclear. Our goal was to investigate changes occurring in the action potential duration (APD) and conduction velocity (CV) in the diabetic rabbit ventricle, and delineate the principal ionic determinants. A rabbit model of alloxan-induced diabetes was utilized. Optical imaging was used to record electrical activity in isolated Langendorff-perfused hearts in normo-, hypo- and hyper-kalemia ([K(+)]o=4, 2, 12 mM respectively). Patch clamp experiments were conducted to record Na(+) current (I(Na)) in isolated ventricular myocytes. The mRNA/protein expression levels for Nav1.5 (the α-subunit of I(Na)) and connexin-43 (Cx43), as well as fibrosis levels were examined. Computer simulations were performed to interpret experimental data. We found that the APD was not different, but the CV was significantly reduced in diabetic hearts in normo-, hypo-, and, hyper-kalemic conditions (13%, 17% and 33% reduction in diabetic vs. control, respectively). The cell capacitance (Cm) was increased (by ~14%), and the density of INa was reduced by ~32% in diabetic compared to control hearts, but the other biophysical properties of I(Na) were unaltered. The mRNA/protein expression levels for Cx43 were unaltered. For Nav1.5, the mRNA expression was not changed, and though the protein level tended to be less in diabetic hearts, this reduction was not statistically significant. Staining showed no difference in fibrosis levels between the control and diabetic ventricles. Computer simulations showed that the reduced magnitude of I(Na) was a key determinant of impaired propagation in the diabetic ventricle, which may have important implications for arrhythmogenesis.

Indexed as

Action PotentialsAnimalsBlotting, WesternComputer SimulationConnexin 43Diabetes Mellitus, ExperimentalFibrosisHeart Conduction SystemHeart VentriclesMaleMyocytes, CardiacPatch-Clamp TechniquesRabbitsReal-Time Polymerase Chain ReactionRNA, MessengerSodiumConnexin 43RNA, MessengerSodiumDiabetes rabbit cardiac electrophysiology Na(+)-current

Identifiers

PMID24412579
PMCPMC4066653
OpenAlexW2094750001

What OpenQuestion holds

Textmetadata
LicenceTDM
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.