The Role of Nitric Oxide Synthase Isoforms in the Cardiovascular Effects of Air Pollution
NCT00845169 · Status: COMPLETED · Phase: NA · Type: INTERVENTIONAL · Enrollment: 16
Last updated 2014-12-02
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.
Conditions
- Endothelial Dysfunction
Interventions
- 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)
Sponsors & Collaborators
-
NHS Lothian
collaborator OTHER_GOV -
Umeå University
collaborator OTHER -
University of Edinburgh
lead OTHER
Principal Investigators
-
Anders Blomberg, MD PhD · Umeå University
-
David E Newby, PhD FRCP · University of Edinburgh
Study Design
- Allocation
- RANDOMIZED
- Purpose
- BASIC_SCIENCE
- Masking
- TRIPLE
- Model
- CROSSOVER
Eligibility
- Min Age
- 18 Years
- Max Age
- 40 Years
- Sex
- ALL
- Healthy Volunteers
- Yes
Timeline & Regulatory
- Start
- 2012-04-30
- Primary Completion
- 2013-06-30
- Completion
- 2013-06-30
Countries
- Sweden
Study Locations
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