Increased nitric oxide in nasal lavage fluid and nitrotyrosine formation in nasal mucosa - indices for severe perennial nasal allergy

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Abstract
The nose contributes the large amount of nitric oxide (NO) to exhaled air. NO is a mediator of vasodilation and yields peroxynitrite (ONOO−) by reacting with superoxide (O−2). ONOO− attacks tyrosine residues to form nitrotyrosine. The aim of this study was to examine the pathophysiological role of NO in nasal mucosa in patients with perennial nasal allergy. We measured nitrite and nitrate (NO−2/NO−3) and 3′,5′-guanosine monophosphate (cyclic GMP) in nasal lavage fluid, and also measured haemoglobin concentration in nasal mucosa as an indicator of blood volume in the patients and healthy volunteers. The deleterious role of NO was also investigated by measuring nitrotyrosine in nasal mucosa. The NO−2/NO−3 concentration in the nasal lavage fluid was 39.5 ± 2.8 μM in healthy volunteers (n = 40), 42.4 ± 3.0 μM in patients with mild allergy (mild group, n = 32), and 88.7 ± 6.6 μM in patients with severe allergy (severe group, n = 61). In the patients whose symptoms were improved with treatment, NO−2/NO−3 levels decreased to 45.7 ± 10.4 μM. The concentration of cyclic GMP in nasal lavage fluid was higher in the severe group than in the healthy volunteers. The mucosal haemoglobin index was 88 ± 4 in the healthy volunteers, 67 ± 4 in the mild group, and 53 ± 2 in the severe group. The formation of nitrotyrosine was expressed 0.58 ± 0.10% to total tyrosine in the severe group (n = 11), but was not found in non-allergy patients (n = 9). The production of NO was increased in patients with perennial nasal allergy, but the blood flow in the nasal mucosa of patients was reduced. Nitrotyrosine formation suggests that there is a process of ONOO−-induced damage in mucosa of patients with the perennial nasal allergy and this damage may limit the dilatation of blood vessels, despite the presence of excessive NO.