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The Role of Nitric Oxide Synthase Isoforms in the Cardiovascular Effects of Air Pollution

Not Applicable
Completed
Conditions
Endothelial Dysfunction
Registration Number
NCT00845169
Lead Sponsor
University of Edinburgh
Brief Summary

Exposure to air pollution has been linked to increased cardiorespiratory morbidity and mortality. The exact component of air pollution that mediates this effect is unknown, but the link is strongest for fine combustion derived particulate matter derived from traffic sources. Recently, it has been demonstrated that inhalation of diesel exhaust impairs vascular vasomotor tone and endogenous fibrinolysis. The mechanism underlying these detrimental vascular is unclear, but is thought to be via oxidative stress and altered bioavailability of endogenous nitric oxide. In these studies we plan to elucidate the role of endogenous nitric oxide synthase isoforms (NO) in the adverse vascular responses observed following exposure to diesel exhaust.

Detailed Description

Not available

Recruitment & Eligibility

Status
COMPLETED
Sex
All
Target Recruitment
16
Inclusion Criteria
  • Healthy volunteers
Exclusion Criteria
  • Regular medication use (except oral contraceptive pill)
  • Current smokers
  • Significant occupational exposure to air pollution
  • Intercurrent illness

Study & Design

Study Type
INTERVENTIONAL
Study Design
CROSSOVER
Primary Outcome Measures
NameTimeMethod
Forearm blood flow measured by venous occlusion plethysmography during intraarterial infusion of nitric oxide synthase inhibitors L-NMMA, SMTC and 1400W and positive control norepinephrine.2-4 hours after exposure
Secondary Outcome Measures
NameTimeMethod
Plasma nitrite concentrationDuring forearm study

Trial Locations

Locations (1)

Umeå University

🇸🇪

Umeå, Sweden

Umeå University
🇸🇪Umeå, Sweden

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