Evidence map›Paper›PMID 23872579›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2013

An autonomic link between inhaled diesel exhaust and impaired cardiac performance: insight from treadmill and dobutamine challenges in heart failure-prone rats.

Alex P Carll, Mehdi S Hazari, Christina M Perez, Q Todd Krantz, Charly J King, Najwa Haykal-Coates, Wayne E Cascio, Daniel L Costa, Aimen K Farraj

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Modification of associations between ambient PMEnvironmental health : a global access science source · 2025
    Observational
  4. Neuroendocrine contribution to sex-related variations in adverse air pollution health effects.Journal of toxicology and environmental health. Part B, Critical reviews · 2024
    Review
  5. Review
  6. Mild allergic airways responses to an environmental mixture increase cardiovascular risk in rats.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Key Characteristics of Cardiovascular Toxicants.Environmental health perspectives · 2021
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Neuroendocrine Regulation of Air Pollution Health Effects: Emerging Insights.Toxicological sciences : an official journal of the Society of Toxicology · 2018
    Review
  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

9 authors at 3 institutions in 1 country.

Alex P Carll* Environmental Sciences and Engineering, University of North Carolina, Chapel Hill, North Carolina 27599;
Mehdi S Hazari
Christina M Perez
Q Todd Krantz
Charly J King
Najwa Haykal-Coates
Wayne E Cascio
Daniel L Costa
Aimen K Farraj
Research Triangle Park Foundation · USEnvironmental Protection Agency · USUniversity of North Carolina at Chapel Hill · US

Funding

TOXICOLOGYT32ES007126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ILONA JASPERS, Bernard E. Weissman · 1985 to 2026
$13.0M
NIEHS NIH HHS T32 ES007126
6 · The paper itself

Abstract

Cardiac disease exacerbation is associated with short-term exposure to vehicular emissions. Diesel exhaust (DE) might impair cardiac performance in part through perturbing efferent sympathetic and parasympathetic autonomic nervous system (ANS) input to the heart. We hypothesized that acute changes in ANS balance mediate decreased cardiac performance upon DE inhalation. Young adult heart failure-prone rats were implanted with radiotelemeters to measure heart rate (HR), HR variability (HRV), blood pressure (BP), core body temperature, and pre-ejection period (PEP, a contractility index). Animals pretreated with sympathetic antagonist (atenolol), parasympathetic antagonist (atropine), or saline were exposed to DE (500 µg/m(3) fine particulate matter, 4h) or filtered air and then treadmill exercise challenged. At 1 day postexposure, separate rats were catheterized for left ventricular pressure (LVP), contractility, and lusitropy and assessed for autonomic influence using the sympathoagonist dobutamine and surgical vagotomy. During DE exposure, atenolol inhibited increases in HR, BP, and contractility, but not body temperature, suggesting a role for sympathetic dominance. During treadmill recovery at 4h post-DE exposure, HR and HRV indicated parasympathetic dominance in saline- and atenolol-pretreated groups that atropine inhibited. Conversely, at treadmill recovery 21h post-DE exposure, HRV and PEP indicated sympathetic dominance and subsequently diminished contractility that only atenolol inhibited. LVP at 1 day postexposure indicated that DE impaired contractility and lusitropy while abolishing parasympathetic-regulated cardiac responses to dobutamine. This is the first evidence that air pollutant inhalation both causes time-dependent oscillations between sympathetic and parasympathetic dominance and decreases cardiac performance via aberrant sympathetic dominance.

Indexed as

Vehicle EmissionsWalkingAnimalsDobutamineElectrocardiographyHeart FailureMaleRatsRats, Inbred SHRDobutamineVehicle Emissionsair pollutionautonomiccardiac functioncardiovasculardiesel exhaustelectrocardiographyheart failureheart rate variabilityratstress test.

Identifiers

PMID23872579
PMCPMC3937599
OpenAlexW2114371456

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.