The Mechanism Of Bacterial Translocation Of Rats After Hemorrhagic Shock And The Role Of Dendritic Cell

The mechanism of bacterial translocation of rats afterhemorrhagic shock and the role of dendritic cellABSTRACTObjective To understand the routes of bacterial translocation, the significance of the routes and the functions of dendritic cells in gut original infective state after hemorrhagic shockMethods E. coil JM 109 with PUC 19 plasmid were implanted in the gut of rats and the severe hemorrhagic shock models of rats were copied by drawing blood from the left femoral artery and keeping the mean arterial blood pressure 5.33 kPa for one hour. At 6, 24, 72 hours after resuscitation, the mesenteric lymph nodes, Peyer's patch, liver, portal blood, peripheral blood were collected and cultivated in LB broth containing I 00~tgIml ampicillin and DNA fingerprint maps were carried out in the positive bacterial culture.3H-TdR was applied to the one-way allogeneic mixed lymphocyte reaction and by this way the stimulating function of dendritic cells, B cells, phagocytes, and peripheral blood mononuclear cells were evaluated.Results The rates and quantities of bacterial translocation by lymphatic system and by blood system was compared as 40/64>20/96(P<0.01) and 31.39 ?15.57>15.59 ?7.l9(P<0.0l) The stimulating function of dendritic cells was enhanced while the stimulating function of the other phagocytes was weaker in the gut original infective state.Conclusion Bacteria could translocate through gut barrier by lymphatic capillary and by venous capillary simultaneously aller hemorrhagic shock. The route of bacterial translocation by blood system played a critical role in the posttraumatic sepsis and subsequential mortality inspite that the rates and numbers of bacteria translocation by blood system were less than that by lymphatic system.The stimulating function of dendritic cells was enhanced in the gut original infective state beyond the expectation and this might relate to the cytokines in the blood in the gut original infective stale after hemorrhagic-3-shock whereas the stimulating function of the other phagocytes, B cells and peripheral blood mononuclear cells was weaker in the gut original infective state and this might be a vital even primary cause which leaded to severe posttraumatic sepsis and mortality.