Evidence map›Paper›PMID 22933026›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2012

Remodeling of intrinsic cardiac neurons: effects of β-adrenergic receptor blockade in guinea pig models of chronic heart disease.

Jean C Hardwick, E Marie Southerland, Allison E Girasole, Shannon E Ryan, Sara Negrotto, Jeffrey L Ardell

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

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  10. Angiotensin receptors alter myocardial infarction-induced remodeling of the guinea pig cardiac plexus.American journal of physiology. Regulatory, integrative and comparative physiology · 2015
    Article
  11. 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

6 authors at 2 institutions in 1 country.

Jean C HardwickDepartment of Biology, Ithaca College, Ithaca, NY 14850, USA. jhardwick@ithaca.edu
E Marie Southerland
Allison E Girasole
Shannon E Ryan
Sara Negrotto
Jeffrey L Ardell
East Tennessee State University · USIthaca College · US

Funding

Myocardial Ischemia Remodels the Cardiac Nervous SystemR01HL071830 · NHLBI · EAST TENNESSEE STATE UNIVERSITY · PI ARDELL, JEFFREY L · 2005 to 2013
$2.8M
Remodeling of the guinea pig intrinsic cardiac plexus with chronic heart diseaseR01HL098589 · NHLBI · ITHACA COLLEGE · PI HARDWICK, JEAN C, SOUTHERLAND, ELIZABETH MARIE · 2010 to 2013
$487k
NHLBI NIH HHS HL-71830NHLBI NIH HHS R01 HL-098589
6 · The paper itself

Abstract

Chronic heart disease induces remodeling of cardiac tissue and associated neuronal components. Treatment of chronic heart disease often involves pharmacological blockade of adrenergic receptors. This study examined the specific changes in neuronal sensitivity of guinea pig intrinsic cardiac neurons to autonomic modulators in animals with chronic cardiac disease, in the presence or absence of adrenergic blockage. Myocardial infarction (MI) was produced by ligature of the coronary artery and associated vein on the dorsal surface of the heart. Pressure overload (PO) was induced by a banding of the descending dorsal aorta (∼20% constriction). Animals were allowed to recover for 2 wk and then implanted with an osmotic pump (Alzet) containing either timolol (2 mg·kg(-1)·day(-1)) or vehicle, for a total of 6-7 wk of drug treatment. At termination, intracellular recordings from individual neurons in whole mounts of the cardiac plexus were used to assess changes in physiological responses. Timolol treatment did not inhibit the increased sensitivity to norepinephrine seen in both MI and PO animals, but it did inhibit the stimulatory effects of angiotensin II on the norepinephrine-induced increases in neuronal excitability. Timolol treatment also inhibited the increase in synaptically evoked action potentials observed in PO animals with stimulation of fiber tract bundles. These results demonstrate that β-adrenergic blockade can inhibit specific aspects of remodeling within the intrinsic cardiac plexus. In addition, this effect was preferentially observed with active cardiac disease states, indicating that the β-receptors were more influential on remodeling during dynamic disease progression.

Indexed as

Adrenergic AgonistsAdrenergic beta-AntagonistsAngiotensin IIAnimalsCholinergic AgentsChronic DiseaseDisease Models, AnimalEvoked PotentialsGuinea PigsHeartHeart DiseasesMaleMyocardial InfarctionNeuronsReceptors, Adrenergic, betaTimololAdrenergic AgonistsAdrenergic beta-AntagonistsAngiotensin IICholinergic AgentsReceptors, Adrenergic, betaTimolol

Identifiers

PMID22933026
PMCPMC3517704
OpenAlexW2154328110

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.