Evidence map›Paper›PMID 24220238›Full record

ArticleAutonomic neuroscience : basic & clinical2014

Dynamic remodeling of the guinea pig intrinsic cardiac plexus induced by chronic myocardial infarction.

Jean C Hardwick, Shannon E Ryan, Eric Beaumont, Jeffrey L Ardell, E Marie Southerland

Abstract read
In one paragraph

Article in Autonomic neuroscience : basic & clinical, 2014. 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
2.8field-weighted citation impact, top 8% 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, 49 citations in OpenAlex.

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  10. Spinal cord neural network interactions: implications for sympathetic control of the porcine heart.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  11. Review
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  13. [Effect of spinal cord stimulation on myocardial ischemia/infarction].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2018
    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

5 authors at 2 institutions in 1 country.

Jean C HardwickDepartment of Biology, Ithaca College, Ithaca, NY 14850, United States. Electronic address: jhardwick@ithaca.edu.
Shannon E RyanDepartment of Biology, Ithaca College, Ithaca, NY 14850, United States.
Eric BeaumontDepartment of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, United States.
Jeffrey L ArdellDepartment of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, United States.
E Marie SoutherlandDepartment of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, United States.
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 HL071830NHLBI NIH HHS R01 HL071830NHLBI NIH HHS R01 HL098589
6 · The paper itself

Abstract

Myocardial infarction (MI) is associated with remodeling of the heart and neurohumoral control systems. The objective of this study was to define time-dependent changes in intrinsic cardiac (IC) neuronal excitability, synaptic efficacy, and neurochemical modulation following MI. MI was produced in guinea pigs by ligation of the coronary artery and associated vein on the dorsal surface of the heart. Animals were recovered for 4, 7, 14, or 50 days. Intracellular voltage recordings were obtained in whole mounts of the cardiac neuronal plexus to determine passive and active neuronal properties of IC neurons. Immunohistochemical analysis demonstrated an immediate and persistent increase in the percentage of IC neurons immunoreactive for neuronal nitric oxide synthase. Examination of individual neuronal properties demonstrated that after hyperpolarizing potentials were significantly decreased in both amplitude and time course of recovery at 7 days post-MI. These parameters returned to control values by 50 days post-MI. Synaptic efficacy, as determined by the stimulation of axonal inputs, was enhanced at 7 days post-MI only. Neuronal excitability in absence of agonist challenge was unchanged following MI. Norepinephrine increased IC excitability to intracellular current injections, a response that was augmented post-MI. Angiotensin II potentiation of norepinephrine and bethanechol-induced excitability, evident in controls, was abolished post-MI. This study demonstrates that MI induces both persistent and transient changes in IC neuronal functions immediately following injury. Alterations in the IC neuronal network, which persist for weeks after the initial insult, may lead to alterations in autonomic signaling and cardiac control.

Indexed as

Angiotensin IIAnimalsAxonsBethanecholChronic DiseaseGuinea PigsHeartIn Vitro TechniquesMaleMembrane PotentialsMyocardial InfarctionNeuronsNitric Oxide Synthase Type INorepinephrineParasympathomimeticsSympathetic Nervous SystemAngiotensin IIBethanecholNitric Oxide Synthase Type INorepinephrineParasympathomimeticsSympathomimeticsVasoconstrictor AgentsAngiotensin IIBethanecholIntrinsic cardiac nervous systemMyocardial infarctionNeuromodulationNorepinephrine

Identifiers

PMID24220238
PMCPMC3944072
OpenAlexW2091045406

What OpenQuestion holds

Textmetadata
LicenceTDM
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.