Evidence map›Paper›PMID 26791829›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2016

Increase in cholinergic modulation with pyridostigmine induces anti-inflammatory cell recruitment soon after acute myocardial infarction in rats.

Juraci Aparecida Rocha, Susan Pereira Ribeiro, Cristiane Miranda França, Otávio Coelho, Gisele Alves, Silvia Lacchini, Esper Georges Kallás, Maria Cláudia Irigoyen, Fernanda M Consolim-Colombo

Open access · greenAbstract read
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 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.9field-weighted citation impact, top 10% 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, 46 citations in OpenAlex.

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  16. Mediation of Cardiac Macrophage ActivityFrontiers in neuroscience · 2020
    Review
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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

9 authors at 2 institutions in 1 country.

Juraci Aparecida RochaHeart Institute (InCor)-Hypertension Unit, Medical School University of São Paulo, São Paulo, Brazil.
Susan Pereira RibeiroUniversity of São Paulo-Medical School University of São Paulo, Laboratory of Clinical Immunology and Allergy, Division of Medicine, São Paulo, Brazil.
Cristiane Miranda FrançaUniversity Nove de Julho, São Paulo, Brazil.
Otávio CoelhoUniversity Nove de Julho, São Paulo, Brazil.
Gisele AlvesUniversity Nove de Julho, São Paulo, Brazil.
Silvia LacchiniBiomedical Sciences Institute, University of São Paulo, São Paulo, Brazil.ORCID http://orcid.org/0000-0002-7937-8473
Esper Georges KallásUniversity of São Paulo-Medical School University of São Paulo, Laboratory of Clinical Immunology and Allergy, Division of Medicine, São Paulo, Brazil.
Maria Cláudia IrigoyenHeart Institute (InCor)-Hypertension Unit, Medical School University of São Paulo, São Paulo, Brazil.
Fernanda M Consolim-ColomboHeart Institute (InCor)-Hypertension Unit, Medical School University of São Paulo, São Paulo, Brazil University Nove de Julho, São Paulo, Brazil fernanda.consolim@incor.com.br.
Universidade de São Paulo · BRUniversidade Nove de Julho · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We tested the hypothesis that an increase in the anti-inflammatory cholinergic pathway, when induced by pyridostigmine (PY), may modulate subtypes of lymphocytes (CD4+, CD8+, FOXP3+) and macrophages (M1/M2) soon after myocardial infarction (MI) in rats. Wistar rats, randomly allocated to receive PY (40 mg·kg(-1)·day(-1)) in drinking water or to stay without treatment, were followed for 4 days and then were subjected to ligation of the left coronary artery. The groups-denominated as the pyridostigmine-treated infarcted (IP) and infarcted control (I) groups-were submitted to euthanasia 3 days after MI; the heart was removed for immunohistochemistry, and the peripheral blood and spleen were collected for flow cytometry analysis. Noninfarcted and untreated rats were used as controls (C Group). Echocardiographic measurements were registered on the second day after MI, and heart rate variability was measured on the third day after MI. The infarcted groups had similar MI areas, degrees of systolic dysfunction, blood pressures, and heart rates. Compared with the I Group, the IP Group showed a significant higher parasympathetic modulation and a lower sympathetic modulation, which were associated with a small, but significant, increase in diastolic function. The IP Group showed a significant increase in M2 macrophages and FOXP3(+)cells in the infarcted and peri-infarcted areas, a significantly higher frequency of circulating Treg cells (CD4(+)CD25(+)FOXP3(+)), and a less extreme decrease in conventional T cells (CD25(+)FOXP3(-)) compared with the I Group. Therefore, increasing cholinergic modulation with PY induces greater anti-inflammatory cell recruitment soon after MY in rats.

Indexed as

AnimalsAnti-Inflammatory AgentsBiomarkersBlood PressureCD8-Positive T-LymphocytesChemotaxis, LeukocyteCholinergic NeuronsCholinesterase InhibitorsDisease Models, AnimalForkhead Transcription FactorsHeart RateInterleukin-2 Receptor alpha SubunitMacrophage ActivationMacrophagesMaleMyocardial InfarctionAnti-Inflammatory AgentsBiomarkersCholinesterase InhibitorsForkhead Transcription FactorsFOXP3 protein, humanIL2RA protein, humanInterleukin-2 Receptor alpha SubunitPyridostigmine Bromideanticholinesterase drugscholinergic anti-inflammatory reflexmacrophage activationmyocardial infarctionT lymphocytes

Identifiers

PMID26791829
PMCPMC4867407
OpenAlexW2331759894

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.