Modeling an acute lung injury by inhalation of lipopolysaccharide-containing ultrafine aerozoles

We try to initialize the acute toxic lung injury by single lipopolysaccharide E. coli О128 : B12 inhalation in 18 rats vs 6 control ones. The ultrafine aerosol was used for better delivery of toxin into respiratory apparatus of lungs. The dynamics of lipopolysaccharide and morphology of the lung through 3, 8 and 24 hours after inhalation was investigated. The classic histology data, and the estimation of surface epithelial density in bronchial wall and alveoli (1/мм 2), bronchial exudate volume and air volume (%), volume density of bronchial and alveolar macrophages (1 /мм 3) have evidenced the development of acute lung injury. In addition to these methods, we applied immunohistochemical assays to reveal the cells and structures expressed CD68, desmin, and alpha-antitrypsin. An atelektasis, exudation in bronchial lumen, intensity and dynamics of vascular and macrophage reactions, damage to the bronchial and alveolar epithelium, and also early migration of myofibroblasts into intraalveolar septa, and suppression of alpha-antitrypsin can be attributed to the morphological criteria of acute lung damage in the presented model. The developed model adequately reflects relevant processes in acute toxic lung injury in humans.