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采用五联悉生大鼠造成创伤后失血性休克和标准全胃肠外营养（ＴＰＮ）支持实验模型，观察休克后不同营养途径对肠屏障功能的影响。结果发现：休克后第８天，与经胃肠道营养（ＴＥＮ）支持组相比，ＴＰＮ支持组各项肠屏障功能指标发生显著变化，表现为肠道菌群紊乱；肠粘膜变薄，微绒毛缩短，粘膜缺损和大量Ｇ－杆菌侵入粘膜和粘膜下层；二胺氧化酶（ＤＡＯ）活性显著下降，肠细胞功能降低。与上述改变相平行，出现肠道细菌易位率增高，氧自由基损伤加重和动物死亡。证实：休克后ＴＰＮ支持出现的感染率增高与肠屏障功能损害密切相关。休克后机体免疫功能抑制，肠屏障功能低下，而ＴＰＮ支持则加强这种有害作用，即休克后ＴＰＮ途径支持可加重肠屏障功能损伤并引发肠源性感染。ＤＡＯ活性测定能在一定程度上反映肠屏障功能状态。
The experimental model of hemorrhagic shock with trauma and standard total parenteral nutrition (TPN) was established by using WXL rats, and the effect of different nutrition pathway on gut barrier function was observed after shock. The results showed that on the 8th day after shock, compared with the gastrointestinal tract nutrition (TEN) support group, the intestinal barrier function indexes of the TPN support group changed significantly, manifested as intestinal flora disturbance; intestinal mucosa thinning, micro Villi shortening, mucosal defects and a large number of G-bacteria invade the mucosa and submucosa; diamine oxidase (DAO) activity was significantly decreased intestinal cell function decreased. In parallel with the above changes, there was an increase in intestinal bacterial translocation rate, increased oxygen free radical damage and animal death. Confirmed: TPN support after shock increased incidence of infection is closely related to intestinal barrier dysfunction. Immune suppression in the body after shock, intestinal barrier dysfunction, and TPN support is to strengthen this harmful effect, that after the shock of TPN pathway support can aggravate intestinal barrier dysfunction and lead to intestinal infection. DAO activity can reflect the intestinal barrier function status to a certain extent.