Evidence map›Paper›PMID 26661096›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2016

Central vs. peripheral neuraxial sympathetic control of porcine ventricular electrophysiology.

Kentaro Yamakawa, Kimberly Howard-Quijano, Wei Zhou, Pradeep Rajendran, Daigo Yagishita, Marmar Vaseghi, Olujimi A Ajijola, J Andrew Armour, Kalyanam Shivkumar, Jeffrey L Ardell and 1 more

Abstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

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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

11 authors.

Kentaro YamakawaDepartment of Anesthesiology, David Geffen School of Medicine, University of California, Los Angeles (UCLA) Health System, Los Angeles, California;
Kimberly Howard-QuijanoDepartment of Anesthesiology, David Geffen School of Medicine, University of California, Los Angeles (UCLA) Health System, Los Angeles, California; Neurocardiology Research Center of Excellence, David Geffen School of Medicine, UCLA Health System, Los Angeles, California.
Wei ZhouDepartment of Anesthesiology, David Geffen School of Medicine, University of California, Los Angeles (UCLA) Health System, Los Angeles, California;
Pradeep RajendranCardiac Arrhythmia Center, David Geffen School of Medicine, UCLA Health System, Los Angeles, California; and Neurocardiology Research Center of Excellence, David Geffen School of Medicine, UCLA Health System, Los Angeles, California.
Daigo YagishitaCardiac Arrhythmia Center, David Geffen School of Medicine, UCLA Health System, Los Angeles, California; and Neurocardiology Research Center of Excellence, David Geffen School of Medicine, UCLA Health System, Los Angeles, California.
Marmar VaseghiCardiac Arrhythmia Center, David Geffen School of Medicine, UCLA Health System, Los Angeles, California; and Neurocardiology Research Center of Excellence, David Geffen School of Medicine, UCLA Health System, Los Angeles, California.
Olujimi A AjijolaCardiac Arrhythmia Center, David Geffen School of Medicine, UCLA Health System, Los Angeles, California; and Neurocardiology Research Center of Excellence, David Geffen School of Medicine, UCLA Health System, Los Angeles, California.
J Andrew ArmourCardiac Arrhythmia Center, David Geffen School of Medicine, UCLA Health System, Los Angeles, California; and Neurocardiology Research Center of Excellence, David Geffen School of Medicine, UCLA Health System, Los Angeles, California.
Kalyanam ShivkumarCardiac Arrhythmia Center, David Geffen School of Medicine, UCLA Health System, Los Angeles, California; and Neurocardiology Research Center of Excellence, David Geffen School of Medicine, UCLA Health System, Los Angeles, California.
Jeffrey L ArdellCardiac Arrhythmia Center, David Geffen School of Medicine, UCLA Health System, Los Angeles, California; and Neurocardiology Research Center of Excellence, David Geffen School of Medicine, UCLA Health System, Los Angeles, California.
Aman MahajanDepartment of Anesthesiology, David Geffen School of Medicine, University of California, Los Angeles (UCLA) Health System, Los Angeles, California; Cardiac Arrhythmia Center, David Geffen School of Medicine, UCLA Health System, Los Angeles, California; and Neurocardiology Research Center of Excellence, David Geffen School of Medicine, UCLA Health System, Los Angeles, California AMahajan@mednet.ucla.edu.

Funding

ELECTROPHYSIOLOGICAL EFFECTS OF NEURAL REMODELING OF THE VENTRICLESR01HL084261 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SHIVKUMAR, KALYANAM · 2006 to 2016
$3.4M
Myocardial Ischemia Remodels the Cardiac Nervous SystemR01HL071830 · NHLBI · EAST TENNESSEE STATE UNIVERSITY · PI ARDELL, JEFFREY L · 2005 to 2013
$2.8M
Antiarrhythmic Mechanisms of Bilateral Cardiac Sympathetic DecentralizationK08HL125730 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI AJIJOLA, OLUJIMI A · 2015 to 2019
$833k
NHLBI NIH HHS K08 HL125730NHLBI NIH HHS R01 HL-084261NHLBI NIH HHS R01 HL-71830
6 · The paper itself

Abstract

Sympathoexcitation is associated with ventricular arrhythmogenesis. The aim of this study was to determine the role of thoracic dorsal root afferent neural inputs to the spinal cord in modulating ventricular sympathetic control of normal heart electrophysiology. We hypothesize that dorsal root afferent input tonically modulates basal and evoked efferent sympathetic control of the heart. A 56-electrode sock placed on the epicardial ventricle in anesthetized Yorkshire pigs (n = 17) recorded electrophysiological function, as well as activation recovery interval (ARI) and dispersion in ARI, at baseline conditions and during stellate ganglion electrical stimulation. Measures were compared between intact states and sequential unilateral T1-T4 dorsal root transection (DRTx), ipsilateral ventral root transection (VRTx), and contralateral dorsal and ventral root transections (DVRTx). Left or right DRTx decreased global basal ARI [Lt.DRTx: 369 ± 12 to 319 ± 13 ms (P < 0.01) and Rt.DRTx: 388 ± 19 to 356 ± 15 ms (P < 0.01)]. Subsequent unilateral VRTx followed by contralateral DRx+VRTx induced no further change. In intact states, left and right stellate ganglion stimulation shortened ARIs (6 ± 2% vs. 17 ± 3%), while increasing dispersion (+139% vs. +88%). There was no difference in magnitude of ARI or dispersion change with stellate stimulation following spinal root transections. Interruption of thoracic spinal afferent signaling results in enhanced basal cardiac sympathoexcitability without diminishing the sympathetic response to stellate ganglion stimulation. This suggests spinal dorsal root transection releases spinal cord-mediated tonic inhibitory control of efferent sympathetic tone, while maintaining intrathoracic cardiocentric neural networks.

Indexed as

Heart RateVentricular Function, LeftAction PotentialsAnimalsArrhythmias, CardiacElectric StimulationFemaleHeart VentriclesLaminectomyMaleModels, AnimalNeural InhibitionNeurons, AfferentNeurons, EfferentSpinal CordSpinal Nerve Rootscardiac neuronal hierarchyspinal cordstellate ganglionsympathetic nervous systemventricular excitability

Identifiers

PMID26661096
PMCPMC4796738

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.