Evidence map›Paper›PMID 20435852›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2010

Mitochondrial KATP channel inhibition blunts arrhythmia protection in ischemic exercised hearts.

John C Quindry, Lindsey Schreiber, Peter Hosick, Jenna Wrieden, J Megan Irwin, Emily Hoyt

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Exercise: Teaching myocytes new tricks.Journal of applied physiology (Bethesda, Md. : 1985) · 2017
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Mechanisms of exercise-induced cardioprotection.Physiology (Bethesda, Md.) · 2014
    Review
  13. Review
  14. Article
  15. Article
  16. Reactive oxygen species are not a required trigger for exercise-induced late preconditioning in the rat heart.American journal of physiology. Regulatory, integrative and comparative physiology · 2012
    Article
  17. Article
  18. Article
  19. Exercise and the cardiovascular system.Cardiology research and practice · 2012
    Article
  20. Article
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

6 authors at 2 institutions in 1 country.

John C QuindryCardioprotection Laboratory, Department of Kinesiology, Auburn University, Auburn, AL 36849, USA. jcq0001@auburn.edu
Lindsey Schreiber
Peter Hosick
Jenna Wrieden
J Megan Irwin
Emily Hoyt
Appalachian State University · USAuburn University · US

Funding

Mitochondrial KATP channels, exercise, and cardioprotectionR15HL087256 · NHLBI · AUBURN UNIVERSITY AT AUBURN · PI QUINDRY, JOHN C · 2007 to 2007
$176k
NHLBI NIH HHS HL087256
6 · The paper itself

Abstract

The mechanisms responsible for anti-arrhythmic protection during ischemia-reperfusion (IR) in exercised hearts are not fully understood. The purpose of this investigation was to examine whether the ATP-sensitive potassium channels in the mitochondria (mito K(ATP)) and sarcolemma (sarc K(ATP)) provide anti-arrhythmic protection in exercised hearts during IR. Male Sprague-Dawley rats were randomly assigned to cardioprotective treadmill exercise or sedentary conditions before IR (I = 20 min, R = 30 min) in vivo. Subsets of exercised animals received pharmacological inhibitors for mito K(ATP) (5-hydroxydecanoate) or sarc K(ATP) (HMR1098) before IR. Blinded analysis of digital ECG tracings revealed that mito K(ATP) inhibition blunted the anti-arrhythmic effects of exercise, while sarc K(ATP) inhibition did not. Endogenous antioxidant enzyme activities for total, CuZn, and Mn superoxide dismutase, catalase, and glutathione peroxidase from ischemic and perfused ventricular tissue were not mitigated by IR, although oxidative stress was elevated in sedentary and mito K(ATP)-inhibited hearts from exercised animals. These findings suggest that the mito K(ATP) channel provides anti-arrhythmic protection as part of exercise-mediated cardioprotection against IR. Furthermore, these data suggest that the observed anti-arrhythmic protection may be associated with preservation of redox balance in exercised hearts.

Indexed as

Physical ExertionAnimalsArrhythmias, CardiacBenzamidesCatalaseDecanoic AcidsDisease Models, AnimalElectrocardiographyGlutathione PeroxidaseHydroxy AcidsKATP ChannelsMaleMitochondria, HeartMyocardial Reperfusion InjuryMyocardiumOxidation-Reduction5-hydroxydecanoic acidBenzamidesCatalaseDecanoic AcidsGlutathione PeroxidaseHMR 1098Hydroxy AcidsKATP Channelsmitochondrial K(ATP) channelPotassium Channel BlockersPotassium ChannelsSuperoxide Dismutase

Identifiers

PMID20435852
PMCPMC2904130
OpenAlexW2158820335

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.