Evidence map›Paper›PMID 24973409›Full record

ArticleThe Journal of physiology2014

Central command dysfunction in rats with heart failure is mediated by brain oxidative stress and normalized by exercise training.

Satoshi Koba, Ichiro Hisatome, Tatsuo Watanabe

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 17% 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

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

  1. Pooled it
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  11. Augmented fear bradycardia in rats with heart failure.The journal of physiological sciences : JPS · 2019
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  18. Modulation of angiotensin II signaling following exercise training in heart failure.American journal of physiology. Heart and circulatory physiology · 2015
    Review
  19. Effects of exercise training on neurovascular control and skeletal myopathy in systolic heart failure.American journal of physiology. Heart and circulatory physiology · 2015
    Review
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

3 authors at 1 institution in 1 country.

Satoshi KobaDivision of Integrative Physiology, Faculty of Medicine, Tottori University, Yonago, Japan skoba@med.tottori-u.ac.jp.
Ichiro HisatomeDivision of Regenerative Medicine and Therapeutics, Graduate School of Medical Science, Tottori University, Yonago, Japan.
Tatsuo WatanabeDivision of Integrative Physiology, Faculty of Medicine, Tottori University, Yonago, Japan.
Tottori University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sympathoexcitation elicited by central command, a parallel activation of the motor and autonomic neural circuits in the brain, has been shown to become exaggerated in chronic heart failure (CHF). The present study tested the hypotheses that oxidative stress in the medulla in CHF plays a role in exaggerating central command-elicited sympathoexcitation, and that exercise training in CHF suppresses central command-elicited sympathoexcitation through its antioxidant effects in the medulla. In decerebrate rats, central command was activated by electrically stimulating the mesencephalic locomotor region (MLR) after neuromuscular blockade. The MLR stimulation at a current intensity greater than locomotion threshold in rats with CHF after myocardial infarction (MI) evoked larger (P < 0.05) increases in renal sympathetic nerve activity and arterial pressure than in sham-operated healthy rats (Sham) and rats with CHF that had completed longterm (8–12 weeks) exercise training (MI + TR). In the Sham and MI + TR rats, bilateral microinjection of a superoxide dismutase (SOD) mimetic Tempol into the rostral ventrolateral medulla (RVLM) had no effects on MLR stimulation-elicited responses. By contrast, in MI rats, Tempol treatment significantly reduced MLR stimulation-elicited responses. In a subset of MI rats, treatment with Tiron, another SOD mimetic, within the RVLM also reduced responses. Superoxide generation in the RVLM, as evaluated by dihydroethidium staining, was enhanced in MI rats compared with that in Sham and MI + TR rats. Collectively, these results support the study hypotheses. We suggest that oxidative stress in the medulla in CHF mediates central command dysfunction, and that exercise training in CHF is capable of normalizing central command dysfunction through its antioxidant effects in the medulla.

Indexed as

Exercise TherapyOxidative Stress1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium SaltAction PotentialsAnimalsAntioxidantsCyclic N-OxidesHeart FailureMaleMedulla OblongataMyocardial InfarctionRatsRats, Sprague-DawleySpin LabelsSuperoxidesSympathetic Nervous System1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium SaltAntioxidantsCyclic N-OxidesSpin LabelsSuperoxidestempol

Identifiers

PMID24973409
PMCPMC4192711
OpenAlexW2097730758

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.