Nitric oxide attenuates platelet-activating factor-induced nasal airway plasma extravasation in healthy subjects
Paranasal sinuses and the nose are important sources of nitric oxide (NO) in humans but the relevance of NO production to the control of nasal airway plasma exudation and its response to inflammatory mediators such as platelet-activating factor (PAF) in healthy subjects is not well known. Design
In this study we aimed to evaluate the effect of the nitric oxide synthase (NOS) inhibitor NGl-arginine methyl ester (l-NAME) on nasal airway plasma extravasation at baseline and after an acute challenge with PAF that induces most symptoms of rhinitis. Eleven healthy subjects were enrolled in the study. Plasma extravasation in the nasal airway was assessed by measuring the albumin content of nasal lavage. Results
PAF challenge caused a significant increase in concentrations of albumin in the nasal lavage fluid (from 0·59 ± 0·13 mg dL−1 to 2·46 ± 0·45 mg dL−1) after placebo. Pretreatment withl-NAME significantly prevented the increase of albumin in the nasal lavage fluid induced by PAF as compared to placebo (from 0·53 ± 0·11 mg dL−1 to 1·70 ± 0·28 mg dL−1; P < 0·005). Conclusion
Topical administration of a NO inhibitor is able to attenuate the nasal airway plasma extravasation induced by PAF, suggesting that NO release in vivo is involved in the nasal response to PAF.