Evidence map›Paper›PMID 22547631›Full record

ArticleThe Journal of physiology2012

Data-based theoretical identification of subcellular calcium compartments and estimation of calcium dynamics in cardiac myocytes.

Leonid Livshitz, Karoly Acsai, Gudrun Antoons, Karin Sipido, Yoram Rudy

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Modeling NaJournal of molecular and cellular cardiology · 2016
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. What can modelling provide to cardiac physiology?The Journal of physiology · 2012
    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

5 authors at 4 institutions in 4 countries.

Leonid LivshitzCardiac Bioelectricity and Arrhythmia Centre, Washington University in St Louis, St Louis, MO 63130-4899, USA.
Karoly Acsai
Gudrun Antoons
Karin Sipido
Yoram Rudy
Washington University in St. Louis · USHungarian Academy of Sciences · HUKU Leuven · BEMedical University of Graz · AT

Funding

CARDIAC EXCITATION AND ARRHYTHMIASR01HL049054 · NHLBI · WASHINGTON UNIVERSITY · PI RUDY, YORAM · 1993 to 2017
$5.8M
INVERSE AND FORWARD PROBLEMS IN ELECTROCARDIOGRAPHYR01HL033343 · NHLBI · WASHINGTON UNIVERSITY · PI RUDY, YORAM · 1985 to 2015
$2.9M
NHLBI NIH HHS R01 HL033343NHLBI NIH HHS R01-HL033343-27NHLBI NIH HHS R01 HL049054NHLBI NIH HHS R01-HL049054-19
6 · The paper itself

Abstract

In cardiac cells, Ca(2+) release flux (J(rel)) via ryanodine receptors (RyRs) from the sarcoplasmic reticulum (SR) has a complex effect on the action potential (AP). Coupling between J(rel) and the AP occurs via L-type Ca(2+) channels (I(Ca)) and the Na(+)/Ca(2+) exchanger (I(NCX)). We used a combined experimental and modelling approach to study interactions between J(rel), I(Ca) and I(NCX) in porcine ventricular myocytes.We tested the hypothesis that during normal uniform J(rel), the interaction between these fluxes can be represented as occurring in two myoplasmic subcompartments for Ca(2+) distribution, one (T-space) associated with RyR and enclosed by the junctional portion of the SR membrane and corresponding T-tubular portion of the sarcolemma, the other (M-space) encompassing the rest of the myoplasm. I(Ca) and I(NCX) were partitioned into subpopulations in the T-space and M-space sarcolemma. We denoted free Ca(2+) concentrations in T-space and M-space Ca(t) and Ca(m), respectively. Experiments were designed to allow separate measurements of I(Ca) and I(NCX) as a function of J(rel). Inclusion of T-space in themodel allowed us to reproduce in silico the following important experimental results: (1) hysteresis of I(NCX) dependence on Ca(m); (2) delay between peak I(NCX) and peak Ca(m) during caffeine application protocol; (3) delay between I(NCX) and Ca(m) during Ca(2+)-induced-Ca(2+)-release; (4) rapid I(Ca) inactivation (within 2 ms) due to J(rel), with magnitude graded as a function of the SR Ca(2+) content; (5) time delay between I(Ca) inactivation due to J(rel) and Ca(m). Partition of 25% NCX in T-space and 75% in M-space provided the best fit to the experimental data. Measured Ca(m) and I(Ca) or I(NCX) were used as input to the model for estimating Ca(t). The actual model-computed Ca(t), obtained by simulating specific experimental protocols, was used as a gold standard for comparison. The model predicted peak Ca(t) in the range of 6–25 μM, with time to equilibrium of Ca(t) with Ca(m) of ~350 ms. These Ca(t) values are in the range of LCC and RyR sensitivity to Ca(2+). An increase of the SR Ca(2+) load increased the time to equilibrium. The I(Ca)-based estimation method was most accurate during the ascending phase of Ca(t). The I(NCX)-based method provided a good estimate for the descending phase of Ca(t). Thus, application of both methods in combination provides the best estimate of the entire Ca(t) time course.

Indexed as

Models, CardiovascularAnimalsCalciumCalcium Channels, L-TypeMyocytes, CardiacRyanodine Receptor Calcium Release ChannelSarcoplasmic ReticulumSodium-Calcium ExchangerSwineCalciumCalcium Channels, L-TypeRyanodine Receptor Calcium Release ChannelSodium-Calcium Exchanger

Identifiers

PMID22547631
PMCPMC3477750
OpenAlexW1496382049

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.