| Severe acute pancreatitis (SAP) is a common acute abdomen in clinic witha rapid onset and dangerous pathogenetic condition. As sap occurred, severeinflammatory response and a large number of liquid exudation will bring the body aboutan injury of intestinal mucosa barrier by the factors of ischemia and hypoxia、ischemia-reperfusion (IR) injury、 a cascade reaction formed by a variety ofinflammatory mediators and cytokines activate and release and then bring about theincrease of intestinal permeability, even bacterial translocation (BT) and endotoxemiaon the basis of the extensive application of broad-spectrum antibiotics as well aslong-term fasting and parenteral nutrition. A variety of harmful substances released withthe blood flow to the body systems、organs, play a Network-like pathogenic effectwhich promote and influence each other, complicated by sepsis and systemicinflammatory response syndrome (SIRS), causing serious “second-strike” to pancreasand other organs. Even to cause multi-system, multi-organ damage, induce and (or)increase the multiple organ dysfunction syndrome (MODS), eventually leading tomultiple organ failure (MSOF) and death. In the disease process of SAP, the gut is notonly a target organ in MSOF, but the initiator. Therefore, damage of the intestinalmucosal barrier function is the start and the key link in this chain reaction, and blockingthis link, to give timely and effective protection of the intestinal mucosal barrierfunction, plays a crucial role in reducing mortality in patients with SAP. With domesticand foreign researchers in-depth understanding of the Mechanisms with the damage ofintestinal barrier, the protection way of the intestinal mucosa can not be certain of oneor several substances, the combined effects between material to the intestinal barrierfunction will be what the Researchers focus. In this review, we summarize studies onmechanisms of injury with intestinal mucosa barrier and clinical progress in SAP. |
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