| ObjectiveIn order to study theoretical basis for the shock treatment, we observed the changes in different stages of serum inflammatory cytokine IL-6, TNF-αand intestinal mucosa S-IgA of severe traumatic shock in rats.MethodsConstructing a traumatic hemorrhagic shock model of rats through trauma and bloodletting. 64 12-week old SD rats were divided randomly into three groups: A(control), B(shock) and C(resuscitation). The group B was divided into 3 subgroups: B-Ⅰ,B-Ⅱ,B-Ⅲaccording to their shock time including 30 minutes, 60 minutes, 90 minutes, while the group C was divided into 4 subgroups: C-Ⅰ,C-Ⅱ,C-Ⅲ,C-Ⅳaccording to the time after their resuscitation including 0h, 1h, 2h and 4h, each group contains 8 rats. Adding equivalent amount of Ringer liquid to the extracted blood to resuscitate through the femoral vein at the speed of 1.0～1.5ml/min in 30 minutes. The success of resuscitation was determined when the blood pressure recovers to 90% of that before bloodletting. The control group will only go through catheterization of cervical artery and vein and femoral vein to obtain material without bloodletting. Other groups obtain materials when various experimental phases are achieved after severe traumatic shock and resuscitation. Enzyme-linked immuno sorbent assay(ELISA)is adopted to measure IL-6, TNF-αand the content of intentinal mucous S-IgA; immunohistochemical staining ABC method is used to detect the expression of S-IgA in villi; HE staining is adopted to observe the morphological changes of intestinal villus. All the data will be processed by SPSS 16.0 software and the relevant statistical results will be presented in mean±SD(?X±S). The control group adopts the analysis of independent samplet inspection.Results1 After traumatic hemorrhagic shock, the TNF-αlevel of rats in portal vein and inferior vena cava don't increase obviously in 30 mins, then TNF-αin portal vein has begun to rise since 60 minutes, which is significantly different from it of the control group(P<0.01). After 90 minutes of shock, TNF-αin inferior vena cava increases evidently, which has a significant difference from the control group(P<0.05). TNF-αlevel reaches the peak value at 1h after resuscitation, which is clearly different from the control group(P<0.01), and then it turns to decline slowly and time-dependently after resuscitation. In addition, the serum TNF-αlevel in portal vein rises ahead of that of inferior vena cave, but it in inferior vena cave is higher than that in portal vein. The IL-6 level of shock rats shows no obvious distinction from the control groups during the 90mins after shock(P>0.05); But it turns to rise immediately at once the shock rats is resuscitated, then continues to rise in a time-dependent manner and reaches a peak value at 2h after resuscitation, which shows a significant difference from control group(P<0.05). Subseqently it begins to decrease gradually, but untill 4h after resuscitation it also higher than that of the control group(P<0.05). The content of IL-6 in inferior vena cava is higher than that of portal vein.2 Intestinal mucosa S-IgA positive cells are shown as brown particles which exist in cytoplasm, and the quantity and the depth of dying stand for the level of expression. At the table 4, it shows the amount of S-IgA+ plasma cells of B-Ⅰgroup continues to reduce significantly until 4hs after successful resuscitation, afterwards it begins to rise, but still lower significantly than the control group(P<0.05). The intestinal mucosa of S-IgA mainly located in the lamina propria of intestinal mucosa. At the table 4, it shows that content of S-IgA begins to reduce significantly at 1h after shock and declines in a time-dependent manner until 4hs after successful resuscitation. And then it begins to pick up slowly, but still obviously different from the control group(P<0.05). Compared with the content of S-IgA, IgA+ plasma cells reduces earlier and faster and both of them begin to recover slowly after 4hs of successful resuscitation.3 According to the gastrointestinal mucous membrane pathology, it shows downy edema, drop and necrosis with the development of shock. But from 2h after resuscitation, some of the bowel mucosa begins to recovery and parts of bowel mucosa has been repaired and the fibre in lamina propria proliferates at 4hs after successful resuscitation.Conclusions1 The construction of model of severe traumatic hemorrhagic shock rats in this research meets the requirements of duplication, controllability, reliability and stability.2 The content of intestinal S-IgA declines during the course of shock. Even if the shock is reversed in time, the content of intestinal S-IgA still rises until 4hs after resuscitation.3 The intestinal IgA+plasma cell and S-IgA are in negative relation with the content of TNF-αand IL-6. With the declination of intestinal IgA+plasma cell and S-IgA, the content of TNF-a and IL-6 in serum increase gradually, which proves that TNF-a and IL-6 are the factors causing inflammation of interior toxin and bacteria displacement. The interaction between TNF-α, IL-6 and S-IgA is a vicious circle, which results in "Waterfall Pattern" cascade reaction of cytokine and the further declination of S-IgA as well as more damage of intestinal tract. |
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