| pubmed-article:12554905 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12554905 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:12554905 | lifeskim:mentions | umls-concept:C0028128 | lld:lifeskim |
| pubmed-article:12554905 | lifeskim:mentions | umls-concept:C0458827 | lld:lifeskim |
| pubmed-article:12554905 | lifeskim:mentions | umls-concept:C0439064 | lld:lifeskim |
| pubmed-article:12554905 | lifeskim:mentions | umls-concept:C0178987 | lld:lifeskim |
| pubmed-article:12554905 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:12554905 | pubmed:dateCreated | 2003-1-29 | lld:pubmed |
| pubmed-article:12554905 | pubmed:abstractText | Nitric oxide is endogenously released in the airways by nitric oxide synthase. Functionally, two isoforms of this enzyme exist: constitutive and inducible. The former seems to protect airways from excessive bronchoconstriction while the latter has a modulatory role in inflammatory disorders of the airways such as asthma. This review explores the physiological and pathophysiological role of endogenous nitric oxide in the airways, and the clinical aspects of monitoring nitric oxide in exhaled air of patients with respiratory disease. | lld:pubmed |
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