EXHALED NITRIC-OXIDE DURING ACUTE CHANGES OF AIRWAYS CALIBER IN ASTHMA

It has been shown that endogenous nitric oxide (NO), measured in exhal ed air, is increased in asthmatic subjects and after allergen challeng e in sensitized animals, NO is also a paracrine molecule with some, th ough weak, bronchodilator effects, However, whether the amount of endo genous NO that originates in the lungs can reflect the degree of bronc hial tone and airways calibre in asthmatic subjects has not yet been i nvestigated, The aim of this study was, therefore, to determine whethe r NO production could be modified by acute changes of airways calibre in mild, nonatopic, asthmatic subjects. NO output was measured in the exhaled air of 14 steroid-free asthmatics, 8 steroid-treated asthmatic s and 21 control subjects, In seven steroid-free asthmatics, exhaled N O was measured after methacholine challenge, and then after salbutamol -induced bronchial dilatation, Exhaled tidal breathing was collected f or 30 s and NO in the exhaled air was measured with a chemiluminescenc e analyser. Both NO concentration and its output were significantly hi gher in the steroid-free asthmatic patients (15.6+/-1.5 parts per bill ion (ppb) and 6.3+/-0.7 nmol . min(-1), respectively) as compared with the control subjects (8.9+/-1.0 ppb and 3.5+/-0.3 nmol . min(-1), res pectively; p<0.001 for both) and with the steroid-treated asthmatic pa tients (11.3+/-3.3 ppb and 3.7+/-0.9 nmol . min(-1), respectively; p<0 .05 for both), Neither methacholine-induced bronchial obstruction nor salbutamol-induced bronchial dilatation caused a significant change in exhaled NO. We conclude that NO production is higher in steroid-free than in steroid-treated asthmatics and in control subjects, Furthermor e, NO production is not affected by acute pharmacologically-induced ch anges of airways calibre in asthmatic subjects, Our results suggest th at NO production is a marker of airways inflammation rather than an en dogenous modulator of bronchial tone in asthma.