| Objective: To observe the effects and mechanism of pretreatment in rats with prostaglandin E1 on liver after hemorrhagic shock and resuscitation in rats(HSR).Methods:Totally 32 male SD rats were randomly divided into four groups (n=8): group A (sham group); group B shock group(B组):rats were killed after 90 min shock; group C(HSR):rats were anesthetized with pentobarbital, the femoral artery puncture bleeding, mean arterial pressure (MAP) decreased (35±5 mmHg), maintained 90 min, the recovery of autologous blood transfusion to maintain MAP 80 ~ 100 mmHg , the production model of hemorrhagic shock followed by resuscitation ; group D(Lipo-PGE1+ HSR):rats were pretreated with Lipo-PGE1 at 10μg / kg dissolved in 0.5 ml saline injection from the femoral vein one hour before HSR. Liver function,NO and ET-1 were measured , pathological changes of liver tissue in each group were observed,the expressions of iNOS and ET-1 of liver tissue were measured at 6 hours by immunohistochemistry after HSR. Data was analyzed by analysis of variance,and P<0.05 was considered as significantly different.Results: Group B : liver cells swells mildly;ALT,AST,LDH and NO, ET-1 were increased to various degrees (P <0.05) than group A,the expressions of liver iNOS and ET-1 were higher than group A (P < 0.05). Liver of Group C shows serious ischemia-reperfusion injury : a large number of vacuolar degeneration of liver cells, sinus congesting and expanding significantly , massive neutrophil exudating in portal area and hepatic sinus. ALT, AST, LDH were significantly increased in Group C compared with Group B;NO and ET-1 were significantly higher compared with Group B .The expressions of liver iNOS and ET-1 increased in Group C ,compared with Group B. Pathological liver injury in group D significantly reduced compared with Group C showing vacuolar degeneration of hepatocytes was reduced, as well as neutrophil in portal area and sinusoids area.Pre-treatment with Lipo-PGE1 markly reduced the expressions of ALT,AST,LDH ([77.88±17.58)vs. (147.88±15.63);(366.38±67.53)vs. (616.13±132.09);(548.88±50.40)vs. (1355.25±455.13);P <0.05],NO and ET-1[(55.13±4.94)vs. (71.75±6.58);(113.00±8.73)vs.(141.80±11.57);P <0.05],which were consitent with decrase in expressions of iNOS and ET-1 6 hours after HSR[(0.116±0.034) vs. (0.225±0.080),(0.198±0.041) vs. (0.292±0.047),P<0.05].Conclusions: Liver injury after hemorrhagic shock was based mainly on reperfusion injury. Pretreatment of Lipo-PGE1 could reduce liver injury after HSR.The mechanisms might be attributed to inhibiting the expressions of iNOS and ET-1, regulating the balance of NO/ET-1 .
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