ArticleEnvironmental health perspectives2008
Impairment of NO-dependent relaxation in intralobar pulmonary arteries: comparison of urban particulate matter and manufactured nanoparticles.
Article in Environmental health perspectives, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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.
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.
Who cites it
25 citing papers in PubMed, 65 citations in OpenAlex.
- Combustion-derived nanoparticulate induces the adverse vascular effects of diesel exhaust inhalation.European heart journal · 2011Trial
- A hypothesis: Potential contributions of metals to the pathogenesis of pulmonary artery hypertension.Life sciences · 2024Review
- Noise, Air, and Heavy Metal Pollution as Risk Factors for Endothelial Dysfunction.European cardiology · 2023Review
- Physical Activity in Polluted Air-Net Benefit or Harm to Cardiovascular Health? A Comprehensive Review.Antioxidants (Basel, Switzerland) · 2021Review
- Inhalation exposure to three-dimensional printer emissions stimulates acute hypertension and microvascular dysfunction.Toxicology and applied pharmacology · 2017Article
- Nanomaterials Versus Ambient Ultrafine Particles: An Opportunity to Exchange Toxicology Knowledge.Environmental health perspectives · 2017Review
- Left ventricular function in relation to chronic residential air pollution in a general population.European journal of preventive cardiology · 2017Article
- The Toxicological Mechanisms of Environmental Soot (Black Carbon) and Carbon Black: Focus on Oxidative Stress and Inflammatory Pathways.Frontiers in immunology · 2017Review
- Heterogeneous Vascular Bed Responses to Pulmonary Titanium Dioxide Nanoparticle Exposure.Frontiers in cardiovascular medicine · 2017Article
- MicroRNA-338-5p modulates pulmonary hypertension-like injuries caused by SOToxicology research · 2016Article
- Titanium Dioxide Particle Type and Concentration Influence the Inflammatory Response in Caco-2 Cells.International journal of molecular sciences · 2016Article
- Inflammation and Vascular Effects after Repeated Intratracheal Instillations of Carbon Black and Lipopolysaccharide.PloS one · 2016Article
- Zn(II) released from zinc oxide nano/micro particles suppresses vasculogenesis in human endothelial colony-forming cells.Toxicology reports · 2015Article
- Perspective: ambient air pollution: inflammatory response and effects on the lung's vasculature.Pulmonary circulation · 2014Review
- Pulmonary cerium dioxide nanoparticle exposure differentially impairs coronary and mesenteric arteriolar reactivity.Cardiovascular toxicology · 2013Article
- Exposure to ambient air fine particulate matter prevents VEGF-induced mobilization of endothelial progenitor cells from the bone marrow.Environmental health perspectives · 2012Article
- Toxicity and cellular uptake of gold nanorods in vascular endothelium and smooth muscles of isolated rat blood vessel: importance of surface modification.Small (Weinheim an der Bergstrasse, Germany) · 2012Article
- Diesel exhaust particulate induces pulmonary and systemic inflammation in rats without impairing endothelial function ex vivo or in vivo.Particle and fibre toxicology · 2012Article
- Modest effect on plaque progression and vasodilatory function in atherosclerosis-prone mice exposed to nanosized TiO(2).Particle and fibre toxicology · 2011Article
- Mechanisms of diesel-induced endothelial nitric oxide synthase dysfunction in coronary arterioles.Environmental health perspectives · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesBecause pulmonary circulation is the primary vascular target of inhaled particulate matter (PM), and nitric oxide is a major vasculoprotective agent, in this study we investigated the effect of various particles on the NO-cyclic guanosine monophosphate (cGMP) pathway in pulmonary arteries.
methodsWe used intrapulmonary arteries and/or endothelial cells, either exposed in vitro to particles or removed from PM-instilled animals for assessment of vasomotricity, cGMP and reactive oxygen species (ROS) levels, and cytokine/chemokine release.
resultsEndothelial NO-dependent relaxation and cGMP accumulation induced by acetylcholine (ACh) were both decreased after 24 hr exposure of rat intrapulmonary arteries to standard reference material 1648 (SRM1648; urban PM). Relaxation due to NO donors was also decreased by SRM1648, whereas responsiveness to cGMP analogue remained unaffected. Unlike SRM1648, ultrafine carbon black and ultrafine and fine titanium dioxide (TiO2) manufactured particles did not impair NO-mediated relaxation. SRM1648-induced decrease in relaxation response to ACh was prevented by dexamethasone (an anti-inflammatory agent) but not by antioxidants. Accordingly, SRM1648 increased the release of proinflammatory mediators (tumor necrosis factor-alpha, interleukin-8) from intrapulmonary arteries or pulmonary artery endothelial cells, but did not elevate ROS levels within intrapulmonary arteries. Decreased relaxation in response to ACh was also evidenced in intrapulmonary arteries removed from rats intratracheally instilled with SRM1648, but not with fine TiO2.
conclusionIn contrast to manufactured particles (including nanoparticles), urban PM impairs NO but not cGMP responsiveness in intrapulmonary arteries. We attribute this effect to oxidative-stress-independent inflammatory response, resulting in decreased guanylyl cyclase activation by NO. Such impairment of the NO pathway may contribute to urban-PM-induced cardiovascular dysfunction.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.