Evidence map›Paper›PMID 26371172›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2015

Vagal nerve stimulation activates vagal afferent fibers that reduce cardiac efferent parasympathetic effects.

Kentaro Yamakawa, Pradeep S Rajendran, Tatsuo Takamiya, Daigo Yagishita, Eileen L So, Aman Mahajan, Kalyanam Shivkumar, Marmar Vaseghi

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

Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

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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 2 institutions in 1 country.

Kentaro YamakawaUniversity of California Los Angeles Neurocardiology Research Center of Excellence, Los Angeles, California; and Department of Anesthesiology, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, California.
Pradeep S RajendranUniversity of California Los Angeles Cardiac Arrhythmia Center, Los Angeles, California; University of California Los Angeles Neurocardiology Research Center of Excellence, Los Angeles, California; and.
Tatsuo TakamiyaUniversity of California Los Angeles Neurocardiology Research Center of Excellence, Los Angeles, California; and Department of Anesthesiology, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, California.
Daigo YagishitaUniversity of California Los Angeles Cardiac Arrhythmia Center, Los Angeles, California; University of California Los Angeles Neurocardiology Research Center of Excellence, Los Angeles, California; and.
Eileen L SoUniversity of California Los Angeles Cardiac Arrhythmia Center, Los Angeles, California; University of California Los Angeles Neurocardiology Research Center of Excellence, Los Angeles, California; and.
Aman MahajanUniversity of California Los Angeles Cardiac Arrhythmia Center, Los Angeles, California; University of California Los Angeles Neurocardiology Research Center of Excellence, Los Angeles, California; and Department of Anesthesiology, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, California.
Kalyanam ShivkumarUniversity of California Los Angeles Cardiac Arrhythmia Center, Los Angeles, California; University of California Los Angeles Neurocardiology Research Center of Excellence, Los Angeles, California; and.
Marmar VaseghiUniversity of California Los Angeles Cardiac Arrhythmia Center, Los Angeles, California; University of California Los Angeles Neurocardiology Research Center of Excellence, Los Angeles, California; and mvaseghi@mednet.ucla.edu.
Texas Cardiac Arrhythmia · USUniversity of California, Los Angeles · US

Funding

ELECTROPHYSIOLOGICAL EFFECTS OF NEURAL REMODELING OF THE VENTRICLESR01HL084261 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SHIVKUMAR, KALYANAM · 2006 to 2016
$3.4M
Training in Molecular, Cellular &Integrative PhysiologyT32GM065823 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TIDBALL, JAMES G · 2003 to 2017
$2.1M
Myocardial infarction alters information processing within the intrinsic cardiac nervous systemF31HL127974 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI RAJENDRAN, PRADEEP SUNDARAM · 2015 to 2017
$72k
NHLBI NIH HHS F31 HL127974NHLBI NIH HHS R01 HL084261NHLBI NIH HHS R01-HL-084261NIGMS NIH HHS T32 GM065823
6 · The paper itself

Abstract

Vagal nerve stimulation (VNS) has been shown to have antiarrhythmic effects, but many of these benefits were demonstrated in the setting of vagal nerve decentralization. The purpose of this study was to evaluate the role of afferent fiber activation during VNS on efferent control of cardiac hemodynamic and electrophysiological parameters. In 37 pigs a 56-electrode sock was placed over the ventricles to record local activation recovery intervals (ARIs), a surrogate of action potential duration. In 12 of 37 animals atropine was given systemically. Right and left VNS were performed under six conditions: both vagal trunks intact (n = 25), ipsilateral right (n = 11), ipsilateral left (n = 14), contralateral right (n = 7), contralateral left (n = 10), and bilateral (n = 25) vagal nerve transection (VNTx). Unilateral VNTx significantly affected heart rate, PR interval, Tau, and global ARIs. Right VNS after ipsilateral VNTx had augmented effects on hemodynamic parameters and increase in ARI, while subsequent bilateral VNTx did not significantly modify this effect (%change in ARI in intact condition 2.2 ± 0.9% vs. ipsilateral VNTx 5.3 ± 1.7% and bilateral VNTx 5.3 ± 0.8%, P < 0.05). Left VNS after left VNTx tended to increase its effects on hemodynamics and ARI response (P = 0.07), but only after bilateral VNTx did these changes reach significance (intact 1.1 ± 0.5% vs. ipsilateral VNTx 3.6 ± 0.7% and bilateral VNTx 6.6 ± 1.6%, P < 0.05 vs. intact). Contralateral VNTx did not modify VNS response. The effect of atropine on ventricular ARI was similar to bilateral VNTx. We found that VNS activates afferent fibers in the ipsilateral vagal nerve, which reflexively inhibit cardiac parasympathetic efferent electrophysiological and hemodynamic effects.

Indexed as

VagotomyVagus Nerve StimulationAction PotentialsAfferent PathwaysAnimalsAtropineEfferent PathwaysFemaleHeartHeart RateHeart VentriclesHemodynamicsMaleParasympathetic Nervous SystemParasympatholyticsSus scrofaAtropineParasympatholyticsafferent cardiac neurotransmissionelectrophysiologyparasympatheticvagotomy

Identifiers

PMID26371172
PMCPMC4666973
OpenAlexW2281452013

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.