Nitric oxide pathway dysfunction mediates diesel exhaust inhalation induced vascular dysfunction in man | Health & Environmental Research Online (HERO)

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Citation
Tags

HERO ID

2265434

Reference Type

Journal Article

Subtype

Abstract

Title

Nitric oxide pathway dysfunction mediates diesel exhaust inhalation induced vascular dysfunction in man

Author(s)

Langrish, JP; Mills, NL; Unosson, J; Barath, S; Soderberg, S; Pourazar, J; Blackwell, S; Megson, IL; Sandstrom, T; Newby, DE; Blomberg, A

Year

2010

Is Peer Reviewed?

Yes

Journal

American Journal of Respiratory and Critical Care Medicine
ISSN: 1073-449X
EISSN: 1535-4970

Volume

181

Page Numbers

A1717

Language

English

DOI

10.1164/ajrccm-conference.2010.181.1_MeetingAbstracts.A1717

Web of Science Id

WOS:000208771000717

Relationship(s)

is part of a larger document 3452678 Proceedings of the American Thoracic Society 2010 International Conference, May 14-19, 2010, New Orleans

Abstract

Rationale.
We have previously shown that diesel exhaust inhalation causes impaired endothelial-dependent vasodilatation that may be driven by changes in nitric oxide (NO) release or bioavailability. In this study we investigated the role of NO in these adverse vascular effects.

Methods.
In a randomised double-blind cross-over trial, 16 healthy non-smoking volunteers (median age 23 years; 9 male, 7 female) were exposed to dilute diesel exhaust (particle concentration ~300 µg/m^3) or filtered air for 1 hour during intermittent exercise. Two hours after exposure, bilateral forearm blood flow was measured using venous occlusion plethysmography during unilateral intrabrachial infusion of acetylcholine (ACh; 5-20µg/min) and sodium nitroprusside (SNP; 2-8µg/min) in the presence of an “NO clamp” (NO synthase inhibitor, L-N-Gmonomethylarginine, 8 µg/min co-infused with the NO donor SNP at 90-900 ng/min titrated to restore basal blood flow).

Results.
Both ACh and SNP caused dose-dependent increases in blood flow (P<0.01 for both) that were similar (Figure) following exposure to filtered air and diesel exhaust.

Conclusion.
In the presence of NO synthase inhibition, and absence of endogenous NO, diesel exhaust inhalation does not cause further vasomotor dysfunction. This suggests that the adverse vascular effects of air pollution are mediated through the L-arginine-NO pathway.

Conference Name

American Thoracic Society 2010 International Conference

Conference Location

New Orleans, LA

Conference Dates

May 14-19, 2010