animal model of acute lung injury induced by oleic acid and lipopolysaccharide

Objective To compare the characteristics of the animal models of acute lung injury induced by oleic acid(OA) and(or) lipopolysaccharide (LPS) in rats.Methods Twenty four male Wistar rats were randomly divided into four groups(n=6):control group (no interventions), group administered LPS only (10 mg/kg, intraperitoneally), group administered OA only (0.15 ml/kg, intravenously), and group administered LPS+OA (OA given 30 minutes after LPS).The mean arterial blood pressure (MAP) and heart rate (HR) were monitored continuously.Blood and tissue samples were collected 120 minutes after the first drug injection.The NF-κB p65, MPO of lung tissue and serum IL-6 were measured respectively.The blood gas analysis, wet to dry ratio (W/D) of right lung and pathological changes were also observed.Results As compared with the control group, the expression of NF-κB p65 and the activity of MPO in lung tissue and serum IL-6 levels were increased in the LPS group, but the W/D ratio and gas exchange were no statistically significant.In contrast, OA caused severe alveolar damage with associated abnormalities in gas exchange and the W/D ratio, but the expression of NF-κB p65 and the activity of MPO in lung tissue and serum IL-6 levels had no change.When given together, LPS and OA acted synergistically to increase the expression of NF-κB p65 and MPO activity in lung tissue and serum IL-6 levels, the W/D ratio and PaCO2 significantly increased and pH and PaO2 markedly decreased.The histopathologic changes of lung tissue showed alveolar hemorrhage, necrosis and proteinaceous alveolar edema.Conclusions Two-hit model of acute lung injury induced by oleic acid combined with lipopolysaccharide is an ideal model for ALI, which mimics clinical manifestations.