【Abstract】Objective: To observe the influences of sevoflurane on pig’s intestinal barrier function in hemorrhagic shock. Methods: Bama miniature pigs (24) were randomly divided into four equal groups （n=6 wells each）using a random number table: sham group (group S), hemorrhagic shock group (group HS), sevoflurane preconditioning group (group Pre /Sev) and sevoflurane post-treatment group (group Post / Sev).Experimental animals were fasted for 8 hours before surgery, intravenous propofol 3mg/Kg from the ear vein, endotrachealing intubation when animal sleep. In group S, only the position of the femoral artery and the jugular vein catheter after anesthesia, vital signs to detect. We built a hemorrhagic shock model in group HS through the femoral artery bleeding after anesthesia and catheterization. In group Pre/Sev, builtting hemorrhagic shock model after preconditioning 2% sevoflurane 30min . In Post / Sev group post –conditioning 2% sevoflurane 30min after a successful hemorrhagic model. Blood samples were collected at prior to anesthesia (T0), after hemorrhagic shock 30min (T1), 1h (T2), 1.5h (T3), 2h (T4 ), 3h (T5), 4h (T6) 7 time points, ELISA was used to detect the change of content of IL-6, TNF-a ,D-lactic acid and I-FABP in Serum. Experimental animals in each group were observed and sacrificed after shock 4h. Histopathological changes in the intestinal tissue was observed by HE staining; Vena cava blood and tissue samples were used to monitor bacterial growth. Results: Compared with group S, the serum TNF-a , IL-6, I-FABP, D-Lac contentions and bacterial translocation rate were significantly increased in group HS, Pre/Sev and Post/Sev (P<0.05). Compared with group HS, the above indices were significantly reduced in group Pre/Sev and Post/Sev (P<0.05). There was no significant difference in the above indices at each time point between group Pre/Sev and group Post/Sev (P > 0.05). These results were confirmed by HE staining. Conclusion: sevoflurane could improve, to some extent, pig’s intestinal barrier function in hemorrhagic shock and this effect is likely related to inhibition of the HS-induced inflammatory response.