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Purpose of this project using a rat model of brain death, brain-dead rat liver explore the mechanism of injury, as well as alprostadil Lipo preparation on brain death after liver injury in rats. For the clinical use of brain-dead donor liver transplant provides a theoretical basis. Methods SD rats were 24 healthy and clean, male or female, weighing 220-280g, were randomly divided into four groups, each 6 that brain death group (B), the application of intracranial pressure method to establish brain death model, the respiratory, circulatory support maintain the experimental animal brain dead state 6 hours; sham operation group (C), except without epidural catheter pressure, the rest dealing with brain death group; intervention group (L1, L2) to establish brain death model, L1 group pumped alprostadil Lipo preparations 20ng · Kg -1 · min -1 , L2 group pumped alprostadil Lipo preparations 40ng · Kg -1 < / sup> · min -1 . Group B, L1 and L2 groups epidural before pressurizing the pressing process, the state of brain death mean arterial pressure; epidural before pressing (T1), confirm brain death (T2), brain death 6h (T3 ), femoral vein blood samples in 2ml, automatic biochemical analyzer serum alanine aminotransferase (alanineaminotransferase, ALT), aspartate aminotransferase (aspartatea minotransferase, AST), radioimmunoassay of serum endothelin - 1 (endothelin-1, ET-1) levels, ELISA method for the determination of tumor necrosis factor-α (tumomecrosis factor-α, TNF-α) levels. Drawn at 6 hours of brain death, cut liver tissue samples embedded fixed sections, HE staining of liver cell damage. Application SPSS13.0 software package data processing, statistical data are expressed as mean ± standard deviation, multiple samples were compared using one-way ANOVA, test of significance level to take a = 0.05. Results 1. Mean arterial pressure (MAP) Change: intracranial pressure before the MAP between the groups was no significant difference P> 0.05; pressurization process, B group, L1 and L2 group was significantly higher than the C group, there were significant difference P <0.05; But B group and L1, L2 were no significant differences in P> 0.05. Brain death state group B, L1 and L2 group MAP than normal status was significantly reduced, but the groups were not significantly different P <0.05. 2.ALT, AST, TNF-α, ET-1 expression levels: at T1, T2, T3 point in time, each experimental group ALT, AST differences were statistically significant, P <0.05; time point at T3, B group, L1 and L2 group and C group were significantly different P <0.05, L1 and L2 were lower than B group, the difference was significant P <0.05, L2 L1 group and no significant difference P> 0.05. 3. morphological changes in the liver: C group at each time point of the light microscope morphology of normal liver cells, stained uniform, no liver cells necrosis, edema; B group hepatocytes lighter staining cytoplasm loose, cell volume increases, part of the liver cells showed obvious edema, vacuolar changes; L1, L2 group of small changes, the basic morphology of normal liver cells edema, vacuolar changes than in group B reduced. Conclusion 1. Applied improved intermittent intracranial pressure method produced slow brain dead rat model can effectively simulate the clinical brain death state. (2) the state of brain death can cause brain dead rat liver injury changed. Rat brain death state hemodynamic changes in blood and inflammatory cytokine release may be caused by brain dead donor liver injury in rats main reason. 3 serum after brain death TNF-α, ET-1 levels may be increased in one of the main causes of liver injury. 4 alprostadil Lipo preparation can significantly reduce the state of brain death liver damage. May be related to protection of sinusoidal endothelial cells and improve hepatic microcirculation, reducing the release of inflammatory cytokines.
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