Evidence map›Paper›PMID 24971358›Full record

ArticleBioMed research international2014

Effect of Ca2+ efflux pathway distribution and exogenous Ca2+ buffers on intracellular Ca2+ dynamics in the rat ventricular myocyte: a simulation study.

Michal Pásek, Jiří Simurda, Clive H Orchard

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

5 citing papers in PubMed, 25 citations in OpenAlex.

  1. Sarcolemmal distribution ofAmerican journal of physiology. Heart and circulatory physiology · 2017
    Article
  2. Article
  3. Altered Na/Ca exchange distribution in ventricular myocytes from failing hearts.American journal of physiology. Heart and circulatory physiology · 2016
    Article
  4. Article
  5. The calcium stored in the sarcoplasmic reticulum acts as a safety mechanism in rainbow trout heart.American journal of physiology. Regulatory, integrative and comparative physiology · 2014
    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

3 authors at 2 institutions in 2 countries.

Michal PásekInstitute of Thermomechanics, Branch Brno, Academy of Science of the Czech Republic, Technická 2, 61669 Brno, Czech Republic ; Department of Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, 62500 Brno, Czech Republic.ORCID 0000-0001-8198-1215
Jiří SimurdaDepartment of Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, 62500 Brno, Czech Republic.
Clive H OrchardSchool of Physiology and Pharmacology, University of Bristol, Bristol BS8 1TD, UK.
Masaryk University · CZUniversity of Bristol · GB

Funding

British Heart Foundation PG/10/91/28644British Heart Foundation RG/12/10/29802
6 · The paper itself

Abstract

We have used a previously published computer model of the rat cardiac ventricular myocyte to investigate the effect of changing the distribution of Ca(2+) efflux pathways (SERCA, Na(+)/Ca(2+) exchange, and sarcolemmal Ca(2+) ATPase) between the dyad and bulk cytoplasm and the effect of adding exogenous Ca(2+) buffers (BAPTA or EGTA), which are used experimentally to differentially buffer Ca(2+) in the dyad and bulk cytoplasm, on cellular Ca(2+) cycling. Increasing the dyadic fraction of a particular Ca(2+) efflux pathway increases the amount of Ca(2+) removed by that pathway, with corresponding changes in Ca(2+) efflux from the bulk cytoplasm. The magnitude of these effects varies with the proportion of the total Ca(2+) removed from the cytoplasm by that pathway. Differences in the response to EGTA and BAPTA, including changes in Ca(2+)-dependent inactivation of the L-type Ca(2+) current, resulted from the buffers acting as slow and fast "shuttles," respectively, removing Ca(2+) from the dyadic space. The data suggest that complex changes in dyadic Ca(2+) and cellular Ca(2+) cycling occur as a result of changes in the location of Ca(2+) removal pathways or the presence of exogenous Ca(2+) buffers, although changing the distribution of Ca(2+) efflux pathways has relatively small effects on the systolic Ca(2+) transient.

Indexed as

AnimalsBuffersCalciumCell CompartmentationComputer SimulationEgtazic AcidHeart VentriclesIntracellular SpaceIon Channel GatingModels, BiologicalMyocytes, CardiacRatsSarcolemmaSodium-Calcium ExchangerTime Factors1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acidBuffersCalciumEgtazic AcidSodium-Calcium Exchanger

Identifiers

PMID24971358
PMCPMC4058148
OpenAlexW1995774223

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.