Evidence map›Paper›PMID 26993230›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2016

Vagus nerve stimulation mitigates intrinsic cardiac neuronal remodeling and cardiac hypertrophy induced by chronic pressure overload in guinea pig.

Eric Beaumont, Gary L Wright, Elizabeth M Southerland, Ying Li, Ray Chui, Bruce H KenKnight, J Andrew Armour, Jeffrey L Ardell

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.5field-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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Autonomic Neuromodulation Acutely Ameliorates Left Ventricular Strain in Humans.Journal of cardiovascular translational research · 2019
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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 3 institutions in 1 country.

Eric BeaumontDepartment of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee;
Gary L WrightDepartment of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee;
Elizabeth M SoutherlandDepartment of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee;
Ying LiDepartment of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee;
Ray ChuiMolecular, Cellular, and Integrative Physiology Program, University of California, Los Angeles, California;
Bruce H KenKnightCyberonics, Inc., Houston, Texas; and.
J Andrew ArmourUCLA Neurocardiology Research Center of Excellence and UCLA Cardiac Arrhythmia Center, Los Angeles, California.
Jeffrey L ArdellMolecular, Cellular, and Integrative Physiology Program, University of California, Los Angeles, California; UCLA Neurocardiology Research Center of Excellence and UCLA Cardiac Arrhythmia Center, Los Angeles, California jardell@mednet.ucla.edu.
East Tennessee State University · USUCLA Health · USUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our objective was to determine whether chronic vagus nerve stimulation (VNS) mitigates pressure overload (PO)-induced remodeling of the cardioneural interface. Guinea pigs (n = 48) were randomized to right or left cervical vagus (RCV or LCV) implant. After 2 wk, chronic left ventricular PO was induced by partial (15-20%) aortic constriction. Of the 31 animals surviving PO induction, 10 were randomized to RCV VNS, 9 to LCV VNS, and 12 to sham VNS. VNS was delivered at 20 Hz and 1.14 ± 0.03 mA at a 22% duty cycle. VNS commenced 10 days after PO induction and was maintained for 40 days. Time-matched controls (n = 9) were evaluated concurrently. Echocardiograms were obtained before and 50 days after PO. At termination, intracellular current-clamp recordings of intrinsic cardiac (IC) neurons were studied in vitro to determine effects of therapy on soma characteristics. Ventricular cardiomyocyte sizes were assessed with histology along with immunoblot analysis of selected proteins in myocardial tissue extracts. In sham-treated animals, PO increased cardiac output (34%, P < 0.004), as well as systolic (114%, P < 0.04) and diastolic (49%, P < 0.002) left ventricular volumes, a hemodynamic response prevented by VNS. PO-induced enhancements of IC synaptic efficacy and muscarinic sensitivity of IC neurons were mitigated by chronic VNS. Increased myocyte size, which doubled in PO (P < 0.05), was mitigated by RCV. PO hypertrophic myocardium displayed decreased glycogen synthase (GS) protein levels and accumulation of the phosphorylated (inactive) form of GS. These PO-induced changes in GS were moderated by left VNS. Chronic VNS targets IC neurons accompanying PO to obtund associated adverse cardiomyocyte remodeling.

Indexed as

Vagus Nerve StimulationVentricular Function, LeftVentricular PressureVentricular RemodelingAnimalsApoptosisDisease Models, AnimalGlycogen SynthaseGuinea PigsHeartHypertrophy, Left VentricularMaleMyocytes, CardiacPhosphorylationSynaptic TransmissionTime FactorsGlycogen Synthaseautonomic regulation therapycardiac hypertrophyguinea pigintrinsic cardiac nervous systempressure overloadvagus nerve stimulation

Identifiers

PMID26993230
PMCPMC4895835
OpenAlexW2298253146

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.