NCT01060930|Completed
Diesel Exhaust Inhalation, Systemic Nitric Oxide Inhibition and Cardiac Output
DISCO
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DISCO
Sponsor study identifier
interventional
14
1 country
1
Study Start
March 2010
Date type not reportedThis date has not been verified as actual or estimated.
Primary Completion
June 2010
Actual (reported)Study Completion
June 2010
Actual (reported)Exposure to combustion-derived fine particulate air pollution is associated with cardiovascular mortality and morbidity. In previous studies, exposure to diesel exhaust (a major constituent of urban particulate air pollution) has been shown to impair two important functions of the vascular endothelium: vascular vasomotor function and endogenous fibrinolysis. Our subsequent studies suggest this impairment of vascular function is mediated by a reduction in nitric oxide bioavailability. In this study we aim to investigate the cardiovascular responses to systemic nitric oxide synthase inhibition following exposure to dilute diesel exhaust.
Registry-reported information. Elapsed time and enrollment totals alone do not measure study progress or recruitment pace.
June 2010
Actual (reported)Click on a node to explore related trials.
Some registry-reported names shown below are not yet linked in this graph.
Dates and qualifiers reported by the registry. Estimated dates do not confirm that a milestone has occurred.
January 28, 2010
Actual (reported)February 2, 2010
Actual (reported)March 2010
Date type not reportedThis date has not been verified as actual or estimated.
June 2010
Actual (reported)June 2010
Actual (reported)Blood pressure response to NO inhibition
Blood pressure will be measured continuously through the vascular study using intra-arterial monitoring
Heart rate response to systemic nitric oxide inhibition
Heart rate will be measured continuously throughout the study period using continous electrocardiography
Central arterial stiffness following NO inhibition
Measured at baseline, and every 5 minutes during the 2-hour vascular study
Cardiac output during NO inhibition
Measured at baseline, and every 5 minutes during the 2-hour vascular study
Plasma nitrite (NO) concentrations
Measured at baseline, and every 15 minutes during the 2-hour vascular study
Platelet activation and platelet-monocyte binding
Measured at baseline, and every 30 minutes during the 2-hour vascular study
1 hour exposure to dilute diesel exhaust \~ 300 mcg/m3 - during intermittent exercise
1 hour exposure to filtered air during intermittent exercise
Intravenous infusion of 3mg/kg L-NMMA (L-NG-monomethyl arginine; NO synthase inhibitor) and nor-epinephrine at 50 ng/kg/min. Each infusion to run over 15 mins and separated by 45 min to allow return to baseline. Drugs infused in a randomised order. During the study, blood pressure will be measured invasively using an intra-arterial radial artery cannula, central arterial stiffness measured using peripheral arterial tonometry and cardiac output using thoracic bioimpedance.
Registry-reported names are shown in full. Names without a link have not yet been matched to a Syfrah profile.
University Hospital Umeå
Umeå, Sweden
Langrish JP, Unosson J, Bosson J, Barath S, Muala A, Blackwell S, Soderberg S, Pourazar J, Megson IL, Treweeke A, Sandstrom T, Newby DE, Blomberg A, Mills NL. Altered nitric oxide bioavailability contributes to diesel exhaust inhalation-induced cardiovascular dysfunction in man. J Am Heart Assoc. 2013 Feb 19;2(1):e004309. doi: 10.1161/JAHA.112.004309.
Jeremy P Langrish, MB BCh MRCP
University of Edinburgh
14 participants (actual enrollment reported by the registry).
First Submitted
January 28, 2010
First Posted
February 2, 2010
Study Start
March 2010
Date type not reportedThis date has not been verified as actual or estimated.
Contact the study team to confirm eligibility.
Primary Completion
June 2010
Actual (reported)Study Completion
June 2010
Actual (reported)Last Updated
December 16, 2011
Record last verified: 2011-04
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Source: ClinicalTrials.gov.
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