Evidence map›Paper›PMID 20382849›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2010

Luminal Ca(2+) content regulates intracellular Ca(2+) release in subepicardial myocytes of intact beating mouse hearts: effect of exogenous buffers.

Dmytro Kornyeyev, Mariano Reyes, Ariel L Escobar

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Role of Reduced Sarco-Endoplasmic Reticulum CaFrontiers in physiology · 2021
    Article
  7. Article
  8. Phase 1 repolarization rate defines CaThe Journal of general physiology · 2019
    Article
  9. Review
  10. Article
  11. Article
  12. A technical review of optical mapping of intracellular calcium within myocardial tissue.American journal of physiology. Heart and circulatory physiology · 2016
    Review
  13. Article
  14. Article
  15. Chasing cardiac physiology and pathology down the CaMKII cascade.American journal of physiology. Heart and circulatory physiology · 2015
    Review
  16. Cardiac alternans and intracellular calcium cycling.Clinical and experimental pharmacology & physiology · 2014
    Review
  17. Article
  18. Article
  19. Calcium alternans in cardiac myocytes: order from disorder.Journal of molecular and cellular cardiology · 2013
    Review
  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

3 authors at 1 institution in 1 country.

Dmytro KornyeyevSchool of Engineering, Univ. of California-Merced, 5200 N. Lake Rd., Merced, CA 95343, USA.
Mariano Reyes
Ariel L Escobar
University of California, Merced · US

Funding

Subcellular Origin of T-wave Alternans in the Beating Mouse HeartR01HL084487 · NHLBI · UNIVERSITY OF CALIFORNIA, MERCED · PI ESCOBAR, ARIEL L · 2007 to 2011
$1.9M
NHLBI NIH HHS R01-HL-084487
6 · The paper itself

Abstract

Ca(+)-induced Ca(2+) release tightly controls the function of ventricular cardiac myocytes under normal and pathological conditions. Two major factors contributing to the regulation of Ca(2+) release are the cytosolic free Ca(2+) concentration and sarcoplasmic reticulum (SR) Ca(2+) content. We hypothesized that the amount of Ca(2+) released from the SR during each heart beat strongly defines the refractoriness of Ca(2+) release. To test this hypothesis, EGTA AM, a high-affinity, slow-association rate Ca(2+) chelator, was used as a tool to modify luminal SR Ca(2+) content. An analysis of the cytosolic and luminal SR Ca(2+) dynamics recorded from the epicardial layer of intact mouse hearts indicated that the presence of EGTA reduced the diastolic SR free Ca(2+) concentration and fraction of SR Ca(2+) depletion during each beat. In addition, this maneuver shortened the refractory period and accelerated the restitution of Ca(2+) release. As a consequence of the accelerated restitution, the frequency dependence of Ca(2+) alternans was significantly shifted toward higher heart rates, suggesting a role of luminal SR Ca(2+) in the genesis of this highly arrhythmogenic phenomenon. Thus, intra-SR Ca(2+) dynamics set the refractoriness and frequency dependence of Ca(2+) transients in subepicardial ventricular myocytes.

Indexed as

AnimalsBuffersCalciumCytosolEgtazic AcidMaleMiceModels, AnimalModels, TheoreticalMyocardial ContractionMyocardiumMyocytes, CardiacPericardiumSarcoplasmic ReticulumTime FactorsBuffersCalciumEGTA acetoxymethyl esterEgtazic Acid

Identifiers

PMID20382849
PMCPMC2886618
OpenAlexW2066535155

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.