The effect of hypothermia on cytokine expression in rats with lipopolysaccharide-induced acute respiratory distress syndrome

Objective To investigate the effect of hypothermia on cytokine expression in rats with lipopolysaccharide- induced acute respiratory distress syndrome (ARDS), and investigate whether or not hypothermia can inhibit inflammatory reaction and attenuated lung injuries, thereby preventing the development of ARDS. Methods A rat model of ARDS was established by intratracheal instillation of lipopolysaccharide (3 mg/ kg, 0.5 ml, LPS) at 16 h after LPS (1 mg/kg, 0.3 ml) intraperitoneal administration. Thirty-two male Sprague Dawley rats were randomly divided into four groups: ARDS + Normalthermia (AN) , ARDS + Hypothermia (AH) , NS+ Normalthermia (NN), and NS + Hypothermia (NH) groups. At 3 h after ARDS, rats were killed by hemorrhage from carotid artery. Lung lavage was performed, tumor necrosis factor α(TNF-α) , interleukin-6 (IL-6) concentrations in BALF were measured using enzyme-linked immunosorbent assay (ELISA) .Results Within (2.3±1.6) h the ARDS model in AN group and AH group was successfully replicated. Compared with the NN group, the concentrations of TNF-α and IL-6 increased significantly in the AN group ( P 0.01) . The (concentrations of TNF-α and IL-6 in the AH group were significantly lower than those in the AN group ( P 0.01). However there were no significant differences in the concentrations of TNF-α and IL-6 between the NN group and the NH group ( P 0.05). Conclusion Hypothermia has inhibitory effect on the expression and release of the pro-inflammatory cytokine (TNF-α, IL-6) in rats with ARDS. Hypothermia may inhibit inflammatory reaction, attenuated lung injuries and serve as a new measure to prevent and treat ARDS.