Evidence map›Paper›PMID 23220155›Full record

ArticleJournal of molecular and cellular cardiology2013

In vivo and in vitro cardiac responses to beta-adrenergic stimulation in volume-overload heart failure.

Anuradha Guggilam, Kirk R Hutchinson, T Aaron West, Amy P Kelly, Maarten L Galantowicz, Amy J Davidoff, Sakthivel Sadayappan, Pamela A Lucchesi

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
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  7. Article
  8. Review
  9. Force development and intracellular CaEuropean journal of pharmacology · 2017
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. The effect of histidine on the contractility and adrenoreactivity of the myocardium of nonpregnant and pregnant rats.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2015
    Article
  15. Article
  16. Myofilament dysfunction as an emerging mechanism of volume overload heart failure.Pflugers Archiv : European journal of physiology · 2014
    Review
  17. An endogenous sensitizer of β adrenergic receptors and its analogs attenuate the inhibition of β adrenergic receptors by propranolol and atenolol in the rat myocardium.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2014
    Article
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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

8 authors at 4 institutions in 1 country.

Anuradha GuggilamCenter for Cardiovascular and Pulmonary Research, The Research Institute at Nationwide Children's Hospital, Columbus, OH, USA.
Kirk R Hutchinson
T Aaron West
Amy P Kelly
Maarten L Galantowicz
Amy J Davidoff
Sakthivel Sadayappan
Pamela A Lucchesi
Nationwide Children's Hospital · USLouisiana State University Health Sciences Center New Orleans · USLoyola University Chicago · USUniversity of New England · US

Funding

Regulation of Vascular Smooth Muscle GrowthR01HL056046 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LUCCHESI, PAMELA A · 2001 to 2011
$3.6M
Reactive Inflammatory Species in Heart FailureR01HL063318 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LUCCHESI, PAMELA A · 1999 to 2006
$2.1M
NHLBI NIH HHS 2R01HL056046NHLBI NIH HHS 2R01HL63318NHLBI NIH HHS R01 HL056046NHLBI NIH HHS R01 HL063318
6 · The paper itself

Abstract

Hearts in volume overload (VO) undergo progressive ventricular hypertrophy resulting in chronic heart failure that is unresponsive to β-adrenergic agonists. This study compared left ventricular (LV) and isolated cardiomyocyte contractility and β-adrenergic responsiveness in rats with end-stage VO heart failure (HF). Adult male Sprague-Dawley rats were studied 21 weeks after aortocaval fistula (ACF) or sham surgery. Echocardiography revealed decreased fractional shortening accompanied by increased LV chamber diameter and decreased eccentric dilatation index at end-stage ACF compared to sham. Hemodynamic measurements showed a decrease in the slope of end-systolic pressure-volume relationship, indicating systolic dysfunction. Isolated LV myocytes from ACF exhibited decreased peak sarcomere shortening and kinetics. Both Ca2+ transient amplitude and kinetics were increased in ACF myocytes, with no change under the integrated Ca2+ curves relating to contraction and relaxation phases. Increases in ryanodine receptor and phospholamban phosphorylation, along with a decrease in SERCA2 levels, were observed in ACF. These changes were associated with decreased expression of β-myosin heavy chain, cardiac troponin I and cardiac myosin binding protein-C. In vivo inotropic responses to β-adrenergic stimulation were attenuated in ACF. Interestingly, ACF myocytes exhibited a similar peak shortening to those of sham in response to a β-adrenergic agonist. The protein expression of the gap junction protein connexin-43 was decreased, although its phosphorylation at Ser-368 increased. These changes were associated with alterations in Src and ZO-1. In summary, these data suggest that the disconnect in β-adrenergic responsiveness between in vivo and in vitro conditions may be associated with altered myofilament Ca2+ sensitivity and connexin-43 degradation.

Indexed as

Adrenergic beta-AgonistsAnimalsCalcium SignalingCells, CulturedConnexin 43Extracellular Signal-Regulated MAP KinasesGene ExpressionHeart FailureHeart VentriclesIsoproterenolKineticsMaleMyocardial ContractionMyocytes, CardiacRatsRats, Sprague-DawleyAdrenergic beta-AgonistsConnexin 43Extracellular Signal-Regulated MAP KinasesGja1 protein, ratIsoproterenolTroponin IVentricular Myosins

Identifiers

PMID23220155
PMCPMC3696990
OpenAlexW1987357336

What OpenQuestion holds

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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.