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

The recruitment status of this study is unknown because the information has not been verified recently.
Verified August 2012 by University of Edinburgh.
Recruitment status was  Not yet recruiting
Sponsor:
Collaborators:
NHS Lothian
Umeå University
Information provided by (Responsible Party):
Jeremy Langrish, University of Edinburgh
ClinicalTrials.gov Identifier:
NCT00845169
First received: February 17, 2009
Last updated: August 3, 2012
Last verified: August 2012

February 17, 2009
August 3, 2012
April 2012
June 2013   (final data collection date for primary outcome measure)
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. [ Time Frame: 2-4 hours after exposure ] [ Designated as safety issue: No ]
Same as current
Complete list of historical versions of study NCT00845169 on ClinicalTrials.gov Archive Site
Plasma nitrite concentration [ Time Frame: During forearm study ] [ Designated as safety issue: No ]
Same as current
Not Provided
Not Provided
 
The Role of Nitric Oxide Synthase Isoforms in the Cardiovascular Effects of Air Pollution
The Role of Nitric Oxide Synthase Isoforms in the Cardiovascular Effects of Air Pollution

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.

Not Provided
Interventional
Not Provided
Allocation: Randomized
Intervention Model: Crossover Assignment
Masking: Double Blind (Subject, Investigator, Outcomes Assessor)
Primary Purpose: Basic Science
Endothelial Dysfunction
Procedure: Forearm vascular study
Forearm venous occlusion plethysmography to measure forearm blood flow during intrabrachial infusion of nitric oxide synthase inhibitors L-NMMA (2-8 µg/min), S-methionyl-L-citrulline (25-200 nmol/min) and 1400W (100-1000 nmol/min) and positive control norepinephrine (60-540 pmol/min)
Other Names:
  • 1400W
  • SMTC
  • L-NMMA
  • Noreadrenaline
  • NorAd
  • Experimental: Diesel Exposure
    1 hour exposure to diesel exhaust at 300 µg/m3 during intermittent exercise
    Intervention: Procedure: Forearm vascular study
  • Experimental: Air Exposure
    1 hour exposure to filtered air during intermittent exercise
    Intervention: Procedure: Forearm vascular study
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Not yet recruiting
16
June 2013
June 2013   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • Healthy volunteers

Exclusion Criteria:

  • Regular medication use (except oral contraceptive pill)
  • Current smokers
  • Significant occupational exposure to air pollution
  • Intercurrent illness
Both
18 Years to 40 Years
Yes
Contact: Anders Blomberg, MD PhD +46 90 785 2234 anders.blomberg@lung.umu.se
Sweden
 
NCT00845169
DNR 08-185M/2
No
Jeremy Langrish, University of Edinburgh
University of Edinburgh
  • NHS Lothian
  • Umeå University
Principal Investigator: Anders Blomberg, MD PhD Umeå University
Principal Investigator: David E Newby, PhD FRCP University of Edinburgh
University of Edinburgh
August 2012

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP