Selective protective effects of nitric oxide inhalation on allergen-induced acute airway reactions in the pig

Background Nitric oxide (NO) is thought to be an important mediator of infl ammatory processes during allergic reactions in the respiratory tract. Objective This study was undertaken to investigate the effects of inhalatio n of NO on the allergen-induced acute airway reactions in the pig. Methods Specific pathogen-free pigs were sensitized with Ascaris suum antig en and challenged with an allergen aerosol during mechanical ventilation an d anaesthesia. One group (n=8) was treated with inhaled NO (20 ppm) which w as given from 30 min before allergen challenge until the experiments were c ompleted at 120 min after challenge. A control group (n=8) did not receive NO (<0.001 ppm). Results Inhalation of 20 ppm NO prevented the fall in arterial pO(2)/FiO(2) levels that was observed in the control group (areas under the curve betwe en 0 and 120 min were 3.7<plus/minus>1.4 kPa/min in NO-treated pigs vs. 15. 9 +/-3.4 in controls, P<0.01, Mann-Whitney U-test) and it decreased baselin e pulmonary arterial pressure (change from time-point -30-0 was 3.1*<plus/m inus>-E-5.3% in the control and -19.9 +/-3.5% in the NO group, P<0.01), whi ch in turn resulted in a lower pulmonary arterial pressure during allergen challenge. NO also caused vasodilatation in the bronchial circulation, resu lting in increased bronchial vascular conductance throughout the experiment . NO inhalation caused a small, but non-significant, reduction in the aller gen-induced bronchoconstrictor response, whereas histamine release, as dete cted in urine, was not changed. Total protein levels in bronchoalveolar lav age (BAL) fluid were significantly decreased in the NO group at I20 min aft er challenge compared with 45 min (373<plus/minus>101 mug/mL vs. 631 +/- 18 4, respectively, P<0.05, Wilcoxon matched pairs test), whereas levels in th e control group did not change between these two time-points (513<plus/minu s>282 vs. 599 +/- 354, not significant). Conclusion These findings indicate that NO inhalation improves ventilation/ perfusion matching and causes some bronchodilatation during the allergen-in duced acute airway reaction, whereas histamine release is not affected. Mor eover, NO inhalation enhanced the clearance of extravasated protein in the airways, possibly through increased bronchial blood flow. Even though some protective effects were seen, this study does not support a therapeutic rol e for exogenous NO in acute allergic reactions.