Evidence map›Paper›PMID 15505083›Full record

ArticleCirculation2004

Rate dependence and regulation of action potential and calcium transient in a canine cardiac ventricular cell model.

Thomas J Hund, Yoram Rudy

Open access · bronzeAbstract read
In one paragraph

Article in Circulation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
153citing papers in PubMed, 1 pooled it
9.6field-weighted citation impact, top 2% 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

153 citing papers in PubMed, 1 synthesis or guideline pooled it, 330 citations in OpenAlex.

  1. Guideline
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Computational Modeling of Cardiac Electrophysiology.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  8. Article
  9. Prokaryotic voltage-gated sodium channels are more effective than endogenous NaAmerican journal of physiology. Heart and circulatory physiology · 2023
    Article
  10. Article
  11. Acute exposure to low-dose bisphenol A delays cardiac repolarization in female canine heart - Implication for proarrhythmic toxicity in large animals.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2023
    Article
  12. Review
  13. Review
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  15. Inducing IJournal of molecular and cellular cardiology · 2022
    Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

93 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Thomas J HundDepartment of Biomedical Engineering, Washington University, St. Louis, MO 63130-4899, USA.
Yoram Rudy
Washington University in St. Louis · US

Funding

CARDIAC EXCITATION AND ARRHYTHMIASR01HL049054 · NHLBI · WASHINGTON UNIVERSITY · PI RUDY, YORAM · 1993 to 2017
$5.8M
INVERSE AND FORWARD PROBLEMS IN ELECTROCARDIOGRAPHYR37HL033343 · NHLBI · WASHINGTON UNIVERSITY · PI RUDY, YORAM · 1998 to 2007
$2.0M
NHLBI NIH HHS R01 HL049054NHLBI NIH HHS R01-HL49054NHLBI NIH HHS R37 HL033343NHLBI NIH HHS R37-HL33343
6 · The paper itself

Abstract

backgroundComputational biology is a powerful tool for elucidating arrhythmogenic mechanisms at the cellular level, where complex interactions between ionic processes determine behavior. A novel theoretical model of the canine ventricular epicardial action potential and calcium cycling was developed and used to investigate ionic mechanisms underlying Ca2+ transient (CaT) and action potential duration (APD) rate dependence. METHODS AND

resultsThe Ca2+/calmodulin-dependent protein kinase (CaMKII) regulatory pathway was integrated into the model, which included a novel Ca2+-release formulation, Ca2+ subspace, dynamic chloride handling, and formulations for major ion currents based on canine ventricular data. Decreasing pacing cycle length from 8000 to 300 ms shortened APD primarily because of I(Ca(L)) reduction, with additional contributions from I(to1), I(NaK), and late I(Na). CaT amplitude increased as cycle length decreased from 8000 to 500 ms. This positive rate-dependent property depended on CaMKII activity.

conclusionsCaMKII is an important determinant of the rate dependence of CaT but not of APD, which depends on ion-channel kinetics. The model of CaMKII regulation may serve as a paradigm for modeling effects of other regulatory pathways on cell function.

Indexed as

Computer SimulationIon TransportModels, Cardiovascular4-AminopyridineAction PotentialsAnimalsCalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium Channels, L-TypeCalcium SignalingCardiac Pacing, ArtificialChloridesComputational BiologyDelayed Rectifier Potassium ChannelsDogs4-AminopyridineCalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium Channels, L-TypeChloridesDelayed Rectifier Potassium ChannelsIsoenzymesPotassiumPotassium Channels, Voltage-GatedRyanodine Receptor Calcium Release ChannelSodiumSodium-Calcium ExchangerSodium ChannelsSodium Chloride SymportersSymporters

Identifiers

PMID15505083
PMCPMC1851913
OpenAlexW2144456050

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.