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Purpose : To investigate the protective effect of sevoflurane against lipopolysaccharide (LPS)-induced acute liver injury (ALI) in amice model. Methods : Seven week-old female BalB/C mice were used. Lung water content and cell count were estimated by standard protocols. Cytokine and chemokine analysis was performed using commercially available kits. Myeloperoxidase activity was evaluated spectrophotometrically while histopathological analysis was carried out by H and E staining. Results : The results revealed that sevoflurane treatment significantly improved gaseous exchange, and reduced lung water content and lung inflammation as evidenced by a decrease in neutrophil migration into BALF (p < 0.01). Sevoflurane also significantly reversed the LPS-triggered suppression of IL-10 in the lung tissues of LPS-treated mice, when compared to saline-treated controls (p < 0.01). It reversed LPS-induced oxidative stress, as demonstrated by increase in total antioxidant capacity (T-AC), catalase (CAT) and superoxide dismutase-1 (SOD-1), as well as an increase in reduced/oxidized glutathione (GSH/GSSG) ratio. In addition, sevoflurane blocked LPS-induced lung tissue injury in ALI mice, and exerted protective effects against acute LPS-induced lung injury. Conclusion : These results suggest that sevoflurane improves gaseous exchange and exerts a protective effect against LPS-triggered lung injury in mice model, most probably due to its antiinflammatory and antioxidant properties. Keywords : Lung injury, Sevoflurane, Respiratory distress, Superoxide dismutase, Liposaccharide

Sevoflurane improves gaseous exchange and exerts protective effects in lipopolysaccharide-induced lung injury in mice models