Evidence map›Paper›PMID 25681431›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2015

Environmentally persistent free radicals compromise left ventricular function during ischemia/reperfusion injury.

Brendan R Burn, Kurt J Varner

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
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  5. Review
  6. Investigating environmentally persistent free radicals (EPFRs) emissions of 3D printing process.Chemical engineering journal (Lausanne, Switzerland : 1996) · 2024
    Article
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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

2 authors at 1 institution in 1 country.

Brendan R BurnDepartment of Pharmacology and Cardiovascular Center of Excellence, Louisiana State University Health Sciences Center, New Orleans, Louisiana.
Kurt J VarnerDepartment of Pharmacology and Cardiovascular Center of Excellence, Louisiana State University Health Sciences Center, New Orleans, Louisiana kvarne@lsuhsc.edu.
Louisiana State University Health Sciences Center New Orleans · US

Funding

Role of microbiota in increased influenza severity due to particulate matter exposureP42ES013648 · NIEHS · LOUISIANA STATE UNIV A&M COL BATON ROUGE · PI LOMNICKI, SLAWO M · 2009 to 2024
$27.6M
Vascular and Cardiac Function Core - "Mentoring in Cardiovascular BiologyP30GM106392 · NIGMS · LSU HEALTH SCIENCES CENTER · PI KAPUSTA, DANIEL R · 2014 to 2018
$5.5M
LSUHSC Summer Internship ProgramT35HL105350 · NHLBI · LSU HEALTH SCIENCES CENTER · PI GREGORY, PAULA ELIZABETH · 2011 to 2015
$119k
NHLBI NIH HHS T35 HL105350NIEHS NIH HHS P42ES013648NIGMS NIH HHS P30GM106392
6 · The paper itself

Abstract

Increases in airborne particulate matter (PM) are linked to increased mortality from myocardial ischemia. PM contains environmentally persistent free radicals (EPFRs) that form as halogenated hydrocarbons chemisorb to transition metal oxide-coated particles, and are capable of sustained redox cycling. We hypothesized that exposure to the EPFR DCB230 would increase cardiac vulnerability to subsequent myocardial ischemia-reperfusion (MI/R) injury. Rats were exposed to DCB230 or vehicle via nose-only inhalation (230 μg max/day) over 30 min/day for 7 days. MI/R or sham MI/R (sham) was initiated 24 h after the final exposure. Following 1 or 7 days of reperfusion, left ventricular (LV) function was assessed and infarct size measured. In vehicle-exposed rats, MI/R injury did not significantly reduce cardiac output (CO), stroke volume (SV), stroke work (SW), end-diastolic volume (EDV), or end-systolic volume (ESV) after 1 day of reperfusion, despite significant reductions in end-systolic pressure (ESP). Preload-recruitable SW (PRSW; contractility) was elevated, presumably to maintain LV function. MI/R 1-day rats exposed to DCB230 also had similarly reduced ESP. Compared with vehicle controls, CO, SV, and SW were significantly reduced in DCB230-exposed MI/R 1-day rats; moreover, PRSW did not increase. DCB230's effects on LV function dissipated within 8 days of exposure. These data show that inhalation of EPFRs can exacerbate the deficits in LV function produced by subsequent MI/R injury. Infarct size was not different between the MI/R groups. We conclude that inhalation of EPFRs can compromise cardiac function during MI/R injury and may help to explain the link between PM and MI/R-related mortality.

Indexed as

AnimalsDisease Models, AnimalFree RadicalsInhalation ExposureMaleMyocardial InfarctionMyocardial Reperfusion InjuryMyocardiumOxidative StressParticle SizeParticulate MatterRats, Sprague-DawleyRisk AssessmentRisk FactorsStroke VolumeTime FactorsFree RadicalsParticulate Mattercardiac toxicityparticulate matterpressure volumerat

Identifiers

PMID25681431
PMCPMC4551132
OpenAlexW2145864270

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.