Evidence map›Paper›PMID 20870565›Full record

ArticleEnvironmental health perspectives2011

Mechanisms of diesel-induced endothelial nitric oxide synthase dysfunction in coronary arterioles.

Tom W Cherng, Michael L Paffett, Olan Jackson-Weaver, Matthew J Campen, Benjimen R Walker, Nancy L Kanagy

Open access · diamondAbstract read
In one paragraph

Article in Environmental health perspectives, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 99 citations in OpenAlex.

  1. Trial
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  11. Air Pollution: Another Threat to HDL Function.International journal of molecular sciences · 2022
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Inflammatory effects of particulate matter air pollution.Environmental science and pollution research international · 2020
    Review
  17. Effects of ambient particulate matter on vascular tissue: a review.Journal of toxicology and environmental health. Part B, Critical reviews · 2020
    Review
  18. Review
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Tom W CherngDepartment of Cell Biology and Physiology, University of New Mexico, Health Sciences Center, Albuquerque, New Mexico 87131, USA.
Michael L Paffett
Olan Jackson-Weaver
Matthew J Campen
Benjimen R Walker
Nancy L Kanagy
University of New Mexico · US

Funding

Mechanisms of Vascular Toxicity from Inhaled ToxicantsR01ES014639 · NIEHS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI CAMPEN, MATTHEW J · 2008 to 2023
$6.7M
Enhancement of Coronary Constriction by Volatile Organic Air ToxicsR56ES014639 · NIEHS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI CAMPEN, MATTHEW J · 2013 to 2013
$148k
NIEHS NIH HHS ES014639NIEHS NIH HHS R01 ES014639NIEHS NIH HHS R56 ES014639
6 · The paper itself

Abstract

BACKGROUND AND

objectiveIncreased air pollutants correlate with increased incidence of cardiovascular disease potentially due to vascular dysfunction. We have reported that acute diesel engine exhaust (DE) exposure enhances vasoconstriction and diminishes acetylcholine (ACh)-induced dilation in coronary arteries in a nitric oxide synthase (NOS)-dependent manner. We hypothesize that acute DE inhalation leads to endothelial dysfunction by uncoupling NOS.

methodsRats inhaled fresh DE (300 µg particulate matter/m3) or filtered air for 5 hr. After off-gassing, intraseptal coronary arteries were isolated and dilation to ACh recorded using videomicroscopy.

resultsArteries from DE-exposed animals dilated less to ACh than arteries from air-exposed animals. NOS inhibition did not affect ACh dilation in control arteries but increased dilation in the DE group, suggesting NOS does not normally contribute to ACh-induced dilation in coronary arteries but does contribute to endothelial dysfunction after DE inhalation. Cyclooxygenase (COX) inhibition did not affect ACh dilation in the DE group, but combined inhibition of NOS and COX diminished dilation in both groups and eliminated intergroup differences, suggesting that the two pathways interact. Superoxide scavenging increased ACh dilation in DE arteries, eliminating differences between groups. Tetrahydrobiopterin (BH4) supplementation with sepiapterin restored ACh-mediated dilation in the DE group in a NOS-dependent manner. Superoxide generation (dihydroethidium staining) was greater in DE arteries, and superoxide scavenging, BH4 supplementation, or NOS inhibition reduced the signal in DE but not air arteries.

conclusionAcute DE exposure appears to uncouple NOS, increasing reactive oxygen species generation and causing endothelial dysfunction, potentially because of depletion of BH4 limiting its bioavailability.

Indexed as

AcetylcholineAir PollutantsAnimalsArteriolesCoronary VesselsEndothelium, VascularMaleNitric Oxide SynthaseProstaglandin-Endoperoxide SynthasesRatsRats, Sprague-DawleyVasodilationVehicle EmissionsAcetylcholineAir PollutantsNitric Oxide SynthaseProstaglandin-Endoperoxide SynthasesVehicle Emissions

Identifiers

PMID20870565
PMCPMC3018507
OpenAlexW2016285140

What OpenQuestion holds

Textmetadata
LicenceCC0
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.