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Exhaled nitric oxide does not provide a marker of vascular endothelial function in healthy humans.
Journal article

Exhaled nitric oxide does not provide a marker of vascular endothelial function in healthy humans.

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  • 1999-09-03
Published in:
  • American journal of respiratory and critical care medicine. - 1999
Administration, Inhalation
Adult
Analysis of Variance
Arginine
Biomarkers
Blood Pressure
Endothelium, Vascular
Enzyme Inhibitors
Heart Rate
Hemodynamics
Humans
Infusions, Intravenous
Luminescent Measurements
Male
Nitric Oxide
Nitric Oxide Synthase
omega-N-Methylarginine
English In the lung, nitric oxide synthase (NOS) has been found in both alveolar epithelial and vascular endothelial cells. Nitric oxide (NO) in the exhaled air stemming from the lower respiratory tract has been claimed to represent a marker of the vascular endothelial NO production. Experimental evidence for this concept, however, is lacking. We compared, in eight healthy volunteers, effects on exhaled NO of epithelial NOS inhibition by N (G)-monomethyl-L-arginine (L-NMMA) inhalation (6 mg/kg over 15 min) with those of endothelial NOS inhibition by L-NMMA infusion (25 microgram/kg/min for 30 min). We also measured blood pressure, heart rate, and L-NMMA plasma concentration. The major new findings were that L-NMMA inhalation which did not have any detectable effect on hemodynamics and L-NMMA plasma concentration, decreased the pulmonary exhaled NO by almost 40%. In contrast, L-NMMA infusion that inhibited endothelial NOS, as evidenced by an increase in blood pressure and a decrease in heart rate, had only a barely detectable effect on exhaled NO (-11 +/- 4% from baseline). Pulmonary exhaled NO is mostly of epithelial rather than endothelial origin, and does not provide a marker for vascular endothelial NO production and/or endothelial function in healthy humans.
Language
  • English
Open access status
closed
Identifiers
Persistent URL
https://sonar.ch/global/documents/130676
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