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. It has been demonstrated that inhalation of diesel exhaust impairs vascular vasomotor tone and endogenous fibrinolysis. Recent studies using an inline retrofit particle trap to reduce the particulate component of exhaust have shown that filtering particles leads to a reversal of the endothelial dysfunction seen after diesel exhaust exposure, and have even suggested an augmentation of vascular function. This raises the question of the cardiovascular effects of the gaseous pollutants, the most abundant of which is nitrogen dioxide. In this study we plan to investigate the cardiovascular effects of nitrogen dioxide exposure.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
TRIPLE
Enrollment
12
Forearm venous occlusion plethysmography to measure forearm blood flow during intrabrachial infusion of vasodilators Acetylcholine (5-20 mg/min), sodium nitroprusside (2-8 µg/min), bradykinin (100-1000 pmol/min) and verapamil (10-100 µg/min)
Umeå University
Umeå, Sweden
Forearm blood flow measured by venous occlusion plethysmography in response to intraarterial vasodilators (acetylcholine, sodium nitroprusside, bradykinin and verapamil)
Time frame: 4-6 hours after exposure
Plasma t-PA concentrations after infusion of bradykinin
Time frame: During forearm study
Exhaled nitric oxide
Time frame: 4-6 hours after exposure
This platform is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional.