Evidence map›Paper›PMID 17001086›Full record

ArticleThe Journal of general physiology2006

Contributions of stretch activation to length-dependent contraction in murine myocardium.

Julian E Stelzer, Richard L Moss

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of general physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
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  7. Molecular regulation of stretch activation.American journal of physiology. Cell physiology · 2022
    Article
  8. Article
  9. Article
  10. Stress-dependent activation of myosin in the heart requires thin filament activation and thick filament mechanosensing.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
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  14. Review
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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.

Julian E StelzerDepartment of Physiology, University of Wisconsin School of Medicine and Public Health, Madison, WI 53706, USA. stelzer@physiology.wisc.edu
Richard L Moss
University of Wisconsin–Madison · US

Funding

RYANODINE RECEPTORS AND ACCESSORY PROTEINSP01HL047053 · NHLBI · UNIVERSITY OF WISCONSIN MADISON · PI MOSS, RICHARD L · 1995 to 2004
$8.5M
My-BP-C Modulation of Cardiac ContractionR37HL082900 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI MOSS, RICHARD L · 2006 to 2015
$6.0M
NHLBI NIH HHS P01 HL047053NHLBI NIH HHS P01 HL-47053NHLBI NIH HHS R37 HL082900NHLBI NIH HHS R37 HL82900PHS HHS PAR-02-110
6 · The paper itself

Abstract

The steep relationship between systolic force production and end diastolic volume (Frank-Starling relationship) in myocardium is a potentially important mechanism by which the work capacity of the heart varies on a beat-to-beat basis, but the molecular basis for the effects of myocardial fiber length on cardiac work are still not well understood. Recent studies have suggested that an intrinsic property of myocardium, stretch activation, contributes to force generation during systolic ejection in myocardium. To examine the role of stretch activation in length dependence of activation we recorded the force responses of murine skinned myocardium to sudden stretches of 1% of muscle length at both short (1.90 microm) and long (2.25 microm) sarcomere lengths (SL). Maximal Ca(2+)-activated force and Ca(2+) sensitivity of force were greater at longer SL, such that more force was produced at a given Ca(2+) concentration. Sudden stretch of myocardium during an otherwise isometric contraction resulted in a concomitant increase in force that quickly decayed to a minimum and was followed by a delayed development of force, i.e., stretch activation, to levels greater than prestretch force. At both maximal and submaximal activations, increased SL significantly reduced the initial rate of force decay following stretch; at submaximal activations (but not at maximal) the rate of delayed force development was accelerated. This combination of mechanical effects of increased SL would be expected to increase force generation during systolic ejection in vivo and prolong the period of ejection. These results suggest that sarcomere length dependence of stretch activation contributes to the steepness of the Frank-Starling relationship in living myocardium.

Indexed as

Ventricular FunctionAnimalsBiomechanical PhenomenaCalciumHeart VentriclesIn Vitro TechniquesKineticsMiceMice, Inbred StrainsMyocardial ContractionStress, MechanicalCalcium

Identifiers

PMID17001086
PMCPMC2151573
OpenAlexW2152768014

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.