Evidence map›Paper›PMID 25375191›Full record

ArticleInternational journal of molecular sciences2014

Role of NADPH oxidase and xanthine oxidase in mediating inducible VT/VF and triggered activity in a canine model of myocardial ischemia.

James B Martins, Ashok K Chaudhary, Shuxia Jiang, Michael Kwofie, Prescott Mackie, Francis J Miller

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 31% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. 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

6 authors at 3 institutions in 1 country.

James B MartinsDivision of Cardiovascular Diseases, Departments of Internal Medicine, University of Iowa and Veterans Affairs Medical Center, Iowa City, Iowa 52242, IA, USA. james-martins@uiowa.edu.
Ashok K ChaudharyDivision of Cardiovascular Diseases, Departments of Internal Medicine, University of Iowa and Veterans Affairs Medical Center, Iowa City, Iowa 52242, IA, USA. ashok-chaudhary@uiowa.edu.
Shuxia JiangDivision of Cardiovascular Diseases, Departments of Internal Medicine, University of Iowa and Veterans Affairs Medical Center, Iowa City, Iowa 52242, IA, USA. shuxia-jiang@uiowa.edu.
Michael KwofieDivision of Cardiovascular Diseases, Departments of Internal Medicine, University of Iowa and Veterans Affairs Medical Center, Iowa City, Iowa 52242, IA, USA. michael-kwofie@uiowa.edu.
Prescott MackieDivision of Cardiovascular Diseases, Departments of Internal Medicine, University of Iowa and Veterans Affairs Medical Center, Iowa City, Iowa 52242, IA, USA. prescott-mackie@uiowa.edu.
Francis J MillerDivision of Cardiovascular Diseases, Departments of Internal Medicine, University of Iowa and Veterans Affairs Medical Center, Iowa City, Iowa 52242, IA, USA. francis-miller@uiowa.edu.
Iowa City VA Medical Center · USUniversity of Iowa · USIowa Diabetes and Endocrinology Research Center · US

Funding

BLRD VA I01 BX001729
6 · The paper itself

Abstract

backgroundVentricular tachycardia or fibrillation (VT/VF) of focal origin due to triggered activity (TA) from delayed afterdepolarizations (DADs) is reproducibly inducible after anterior coronary artery occlusion. Both VT/VF and TA can be blocked by reducing reactive oxygen species (ROS). We tested the hypothesis that inhibition of NADPH oxidase and xanthine oxidase would block VT/VF.

methods69 dogs received apocynin (APO), 4 mg/kg intraveneously (IV), oxypurinol (OXY), 4 mg/kg IV, or both APO and OXY (BOTH) agents, or saline 3 h after coronary occlusion. Endocardium from ischemic sites (3-D mapping) was sampled for Rac1 (GTP-binding protein in membrane NADPH oxidase) activation or standard microelectrode techniques. Results (mean±SE, * p<0.05): VT/VF originating from ischemic zones was blocked by APO in 6/10 *, OXY in 4/9 *, BOTH in 5/8 * or saline in 1/27; 11/16 VT/VFs blocked were focal. In isolated myocardium, TA was blocked by APO (10(-6) M) or OXY (10(-8) M). Rac1 levels in ischemic endocardium were decreased by APO or OXY.

conclusionAPO and OXY suppressed focal VT/VF due to DADs, but the combination of the drugs was not more effective than either alone. Both drugs inhibited ischemic Rac1 with inhibition by OXY suggesting ROS-induced ROS. The inability to totally prevent VT/VF suggests that other mechanisms also contribute to ischemic VT.

Indexed as

AcetophenonesAction PotentialsAnimalsBlotting, WesternDisease Models, AnimalDogsFemaleMaleMyocardial IschemiaNADPH OxidasesOxypurinolrac1 GTP-Binding ProteinTachycardia, VentricularUltrasonographyVentricular FibrillationXanthine OxidaseAcetophenonesacetovanilloneNADPH OxidasesOxypurinolrac1 GTP-Binding ProteinXanthine Oxidase

Identifiers

PMID25375191
PMCPMC4264157
OpenAlexW1970528352

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.