Airway reactivity, inflammatory cell influx and nitric oxide in guinea-pig airways after lipopolysaccharide inhalation

Abstract

1. The aim of this study was to investigate the relationship between airway reactivity, leukocyte influx and nitric oxide (NO), in conscious guinea-pigs after aerosolized lipopolysaccharide (LPS) exposure. 2. Inhaled histamine (1 mM, 20 s), causing no bronchoconstriction before LPS exposure (30 microg ml(-1), 1 h), caused bronchoconstriction at 0.5 and 1 h (P:0.05). When L-NAME inhalation followed LPS, AHR was prolonged from 1 h to at least 4 h (P:<0.01). 6. In summary, aerosolized LPS inhalation caused neutrophil and macrophage airways infiltration, and an early development of AHR followed 48 h later by AHOR to histamine. AHR and AHOR coincided with a respective reduction and elevation in airways NO (metabolites). Thus, NO may aid recovery from AHR, as inhibition of its production prolongs AHR. However, NO deficiency alone is not responsible for LPS-induced AHR.