We investigated if healthy subjects could release NO upon hyperosmolar challenge as a defence mechanism, and whether asthmatics with atopy showed an altered response. A plot of NO output versus flow rate was used to calculate the alveolar level and the NO-flux from the airways. The asthmatics had a higher NO output and this was due to an increased NO-flux from the airways, 86±30 nl min-1 compared with control 21±2 nl min-1 (P<0.05). The alveolar NO levels showed no difference. In response to a dry powder of mannitol the exhaled NO concentration decreased in asthmatics by 37±7%, but increased in the control by 9±4% (P<0.001). The FEV1.0 decreased 13±2% and airway conductance 42±7% in asthmatics and in the controls 2±1% and 0±7%, respectively (P<0.001). We conclude that asthmatics have an altered response to mannitol challenge in regards to exhaled NO. This may result from down regulation of constitutive NO production as a result of high levels of NO flux from the airways.
- Disease, asthma
- Mammals, humans
- Mediator, NO
- Pharmacological agents, mannitol
- Upper airways, inflammation
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine