| ObjectiveThe function of body immune system will be compromised in traumatic hemorrhagic shock, with the damage of intestinal barrier function. Even with a successful resuscitation, the body immunity and intestinal functions may not be recovered simultaneously because the intestinal mucosa and small intestine villa is the most sensitive parts to ischemia and hypoxia, with the latest repair. The study is to explore the changes in body immune function and intestinal immune barrier function in traumatic hemorrhagic shock rats by examination of peripheral blood lymphocyte subsets (CD4~+, CD8~+, CD4~+/ CD8~+) and immunosuppressive acidic protein (IAP), endotoxin, in order to provide the theoretical basis for clinical practice.Materials and method48 male SD rats, with the body weight of 300±10g, were randomly divided into 2 groups: the normal controls (group 1, n=8) and the trauma-hemorrhagic shock group (group 2, n=40). Group 2 were subdivided in 5 subgroups (n=8). Connulation of cervical artery and vein were undergone for monitoring blood pressure and taking blood samples in control group without shock. The shock model was induced in group 2 by making fracture and taking out blood through femoral artery to keep the mean arterial pressure of 40±5 mmHg. The animals of group 2 were killed at 0, 1, 2, 3, 4 and 5 hours after shock separately, and the tissue of intestinal mucosa and blood samples was taken at each time point. The percentage of the subsets of T lymphocyte(CD4~+,CD8~+,CD4~+/CD8~+) were measured by FCM. The expression of s-IgA in the intestinal tissue and the levels of endotoxin and IAP in plasma were examined by ELISA . The morphologic changes of intestinal mucosa were examined under optical microscope. Result1. Vital signs: Heart rate went faster significantly as the mean arterial pressure (MAP) dropped and maintained in 40±5mmHg , compared with the control group (P <0.01). As the shock prolonged, rectal temperature decline significantly (P <0.01). The rats in normal contro1 group were all survival, while some of the rats in all shock subgroups died and there were different death rates among the subgroups but had no statistical significance (P>0.05).2. The expression of CD4 and CD4/CD8 ratio were significantly decreased (P <0.05 in subgroupⅡ-A, P<0.01 in other subgroups). The expression of CD8 in peripheral blood were significantly increased in all shock rats, compared with controls(P<0.01).3. The levels of endotoxin were much higher at all phases aftershock than those in controls (P<0.01), and the levels of IAP in plasma went up gradually as shock prolonged, with the significant difference from those of controls(P<0.01).4.The numbers of CD4~+ T lymphocytes were negatively correlated with the plasma concentrations of IAP and LPS ( r1=-0.979, r2=-0.890, P <0.05) in shock group . The value of CD4~+/CD8~+ were negatively correlated with the plasma concentrations of LPS (r 3=-0. 966, P <0. 01) in shock group .5. The pathological damages of small intestinal mucous went more severe gradually as the period of shock prolonged.The amount of intestinal villi went less and the height and thickness went lower and thinner accompanied with the morphological abnormal changes. There were little pathological changes seen in control group.Conclusion1. The declining of anal temperature and the increase of heart rate with the time prolongation of the shock is coincident with the body stress responds to shock.2. The declining of CD4~+ T lymphocytes and the inclining of CD8~+ T lymphocytes with the time prolongation of the shock result in the decrease of the CD4~+/ CD8~+value, which means the depression of the cell immunity during shock in rats. The increase of blood endotoxin and IAP is negatively correlated with the CD4~+/CD8~+ value significantly, which implies endotoxin and IAP may be one of the relative index in depression of body cell immunity after shock.3. The morphological and structural damages of intestinal mucosa and the increase of the permeability of intestinal epithelial cells are the principle condition of endotoxin dislocation.
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