Evidence map›Paper›PMID 23525434›Full record

Trial reportJournal of the American Heart Association2013

Altered nitric oxide bioavailability contributes to diesel exhaust inhalation-induced cardiovascular dysfunction in man.

Jeremy P Langrish, Jon Unosson, Jenny Bosson, Stefan Barath, Ala Muala, Scott Blackwell, Stefan Söderberg, Jamshid Pourazar, Ian L Megson, Andrew Treweeke and 4 more

2 registry-linked trialsOpen access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Journal of the American Heart Association, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 44 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 2 pooled it
7.2field-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.

NCT00845767 nacompletednot on this map

The Cardiovascular Effects of Air Pollution: the Role of Nitric Oxide

TypeinterventionalSponsorUniversity of EdinburghRan2009 to 2009Enrolled16ConditionsEndothelial DysfunctionArmsForearm Vascular Study
NCT01060930 nacompletednot on this map

Diesel Exhaust Inhalation, Systemic Nitric Oxide Inhibition and Cardiac Output

TypeinterventionalSponsorUniversity of EdinburghRan2010 to 2010Enrolled14ConditionsVascular Function in Healthy VolunteersArmsIntravenous infusion of L-NMMA and Nor-epinephrine
3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 90 citations in OpenAlex.

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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

14 authors at 3 institutions in 2 countries.

Jeremy P LangrishUniversity/British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK.
Jon Unosson
Jenny Bosson
Stefan Barath
Ala Muala
Scott Blackwell
Stefan Söderberg
Jamshid Pourazar
Ian L Megson
Andrew Treweeke
Thomas Sandström
David E Newby
Anders Blomberg
Nicholas L Mills
Umeå University · SEUniversity of Edinburgh · GBGlasgow Royal Infirmary · GB

Funding

British Heart Foundation FS/07/048British Heart Foundation FS/10/024/28266British Heart Foundation RG/10/9/28286
6 · The paper itself

Abstract

backgroundDiesel exhaust inhalation causes cardiovascular dysfunction including impaired vascular reactivity, increased blood pressure, and arterial stiffness. We investigated the role of nitric oxide (NO) bioavailability in mediating these effects. METHODS AND

resultsIn 2 randomized double-blind crossover studies, healthy nonsmokers were exposed to diesel exhaust or filtered air. Study 1: Bilateral forearm blood flow was measured during intrabrachial infusions of acetylcholine (ACh; 5 to 20 μg/min) and sodium nitroprusside (SNP; 2 to 8 μg/min) in the presence of the NO clamp (NO synthase inhibitor N(G)-monomethyl-l-arginine (l-NMMA) 8 μg/min coinfused with the NO donor SNP at 90 to 540 ng/min to restore basal blood flow). Study 2: Blood pressure, arterial stiffness, and cardiac output were measured during systemic NO synthase inhibition with intravenous l-NMMA (3 mg/kg). Following diesel exhaust inhalation, plasma nitrite concentrations were increased (68±48 versus 41±32 nmol/L; P=0.006) despite similar l-NMMA-induced reductions in basal blood flow (-20.6±14.7% versus -21.1±14.6%; P=0.559) compared to air. In the presence of the NO clamp, ACh and SNP caused dose-dependent vasodilatation that was not affected by diesel exhaust inhalation (P>0.05 for both). Following exposure to diesel exhaust, l-NMMA caused a greater increase in blood pressure (P=0.048) and central arterial stiffness (P=0.007), but reductions in cardiac output and increases in systemic vascular resistance (P>0.05 for both) were similar to those seen with filtered air.

conclusionsDiesel exhaust inhalation disturbs normal vascular homeostasis with enhanced NO generation unable to compensate for excess consumption. We suggest the adverse cardiovascular effects of air pollution are, in part, mediated through reduced NO bioavailability. CLINICAL

trial registrationURL: http://www.ClinicalTrials.gov. Unique identifiers: NCT00845767 and NCT01060930.

Indexed as

AdultAir PollutantsArginineBiological AvailabilityBlood PressureCardiac OutputCardiovascular DiseasesCross-Over StudiesDose-Response Relationship, DrugDouble-Blind MethodEnzyme InhibitorsFemaleForearmHemodynamicsHumansInhalation ExposureAir PollutantsArginineEnzyme InhibitorsNitric OxideNitric Oxide DonorsNitric Oxide SynthaseNitritesVasodilator AgentsVehicle Emissions

Identifiers

PMID23525434
PMCPMC3603248
OpenAlexW2137010537

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.