Evidence map›Paper›PMID 28740186›Full record

ArticleScientific reports2017

Carotid sinus nerve electrical stimulation in conscious rats attenuates systemic inflammation via chemoreceptor activation.

Fernanda Machado Santos-Almeida, Gean Domingos-Souza, César A Meschiari, Laura Campos Fávaro, Christiane Becari, Jaci A Castania, Alexandre Lopes, Thiago M Cunha, Davi J A Moraes, Fernando Q Cunha and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 39 citations in OpenAlex.

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  11. The Regulation Effect ofMediators of inflammation · 2021
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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

14 authors at 3 institutions in 2 countries.

Fernanda Machado Santos-AlmeidaDepartment of Physiology, Ribeirão Preto Medical School - University of São Paulo, Ribeirão, Preto, 14049-900, Brazil.
Gean Domingos-SouzaDepartment of Physiology, Ribeirão Preto Medical School - University of São Paulo, Ribeirão, Preto, 14049-900, Brazil.
César A MeschiariDepartment of Physiology, Ribeirão Preto Medical School - University of São Paulo, Ribeirão, Preto, 14049-900, Brazil.
Laura Campos FávaroDepartment of Physiology, Ribeirão Preto Medical School - University of São Paulo, Ribeirão, Preto, 14049-900, Brazil.
Christiane BecariDepartment of Physiology, Ribeirão Preto Medical School - University of São Paulo, Ribeirão, Preto, 14049-900, Brazil.
Jaci A CastaniaDepartment of Physiology, Ribeirão Preto Medical School - University of São Paulo, Ribeirão, Preto, 14049-900, Brazil.
Alexandre LopesDepartment of Pharmacology, Medical School of Ribeirão Preto - University of São Paulo, Ribeirão, Preto, 14049-900, Brazil.
Thiago M CunhaDepartment of Pharmacology, Medical School of Ribeirão Preto - University of São Paulo, Ribeirão, Preto, 14049-900, Brazil.
Davi J A MoraesDepartment of Physiology, Ribeirão Preto Medical School - University of São Paulo, Ribeirão, Preto, 14049-900, Brazil.
Fernando Q CunhaDepartment of Pharmacology, Medical School of Ribeirão Preto - University of São Paulo, Ribeirão, Preto, 14049-900, Brazil.
Luis UlloaCenter of Immunology and Inflammation. Rutgers- New Jersey Medical School, Rutgers University, Newark, NJ, 07103, USA.
Alexandre KanashiroDepartment of Pharmacology, Medical School of Ribeirão Preto - University of São Paulo, Ribeirão, Preto, 14049-900, Brazil.ORCID 0000-0003-0367-7503
Geisa C S V TeziniDepartment of Physiology, Ribeirão Preto Medical School - University of São Paulo, Ribeirão, Preto, 14049-900, Brazil.
Helio C SalgadoDepartment of Physiology, Ribeirão Preto Medical School - University of São Paulo, Ribeirão, Preto, 14049-900, Brazil. hcsalgado@fmrp.usp.br.
Universidade de São Paulo · BRUniversidade de Ribeirão Preto · BRRutgers, The State University of New Jersey · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies demonstrated a critical functional connection between the autonomic (sympathetic and parasympathetic) nervous and the immune systems. The carotid sinus nerve (CSN) conveys electrical signals from the chemoreceptors of the carotid bifurcation to the central nervous system where the stimuli are processed to activate sympathetic and parasympathetic efferent signals. Here, we reported that chemoreflex activation via electrical CSN stimulation, in conscious rats, controls the innate immune response to lipopolysaccharide attenuating the plasma levels of inflammatory cytokines such as tumor necrosis factor (TNF), interleukin 1β (IL-1β) and interleukin 6 (IL-6). By contrast, the chemoreflex stimulation increases the plasma levels of anti-inflammatory cytokine interleukin 10 (IL-10). This chemoreflex anti-inflammatory network was abrogated by carotid chemoreceptor denervation and by pharmacological blockade of either sympathetic - propranolol - or parasympathetic - methylatropine - signals. The chemoreflex stimulation as well as the surgical and pharmacological procedures were confirmed by real-time recording of hemodynamic parameters [pulsatile arterial pressure (PAP) and heart rate (HR)]. These results reveal, in conscious animals, a novel mechanism of neuromodulation mediated by the carotid chemoreceptors and involving both the sympathetic and parasympathetic systems.

Indexed as

Electric Stimulation TherapyAnimalsCarotid SinusChemoreceptor CellsConsciousnessCytokinesImmunity, InnateInflammationMaleRatsRats, WistarSympathetic Nervous SystemCytokines

Identifiers

PMID28740186
PMCPMC5524712
OpenAlexW2739300633

What OpenQuestion holds

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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.