重症急性胰腺炎合并胃肠损害机制的研究进展

发布时间：2018-04-27 20:34

  本文选题：重症急性胰腺炎 + 胃肠动力障碍　； 参考：《山东医药》2015年45期

【摘要】：急性胰腺炎尤其是重症急性胰腺炎(SAP)患者早期常出现胃肠功能障碍和黏膜病变。SAP并胃肠动力障碍与神经因素、NO过量、胃肠激素变化、炎症介质过量表达、消化系Cajal间质细胞缺失、胰腺炎相关性腹水等有关,SAP并发消化性溃疡的机制仍不完全清楚,多数研究认为与胰腺本身病变所致的黏膜损害因素加重和抗损害能力的削弱有关。胰腺坏死、脓毒症、APACHEⅡ评分、胰腺脓肿、胰腺囊肿和器官衰竭均是SAP合并消化道出血的高危因素。
[Abstract]:In patients with acute pancreatitis, especially severe acute pancreatitis (SAP), gastrointestinal dysfunction and mucosal lesion. SAP with gastrointestinal motility disorder and neurologic factors such as no excess, gastrointestinal hormone changes, and inflammatory mediators overexpression were often found in the early stage of acute pancreatitis, especially severe acute pancreatitis (SAP). The mechanisms associated with peptic ulcer in digestive system, such as interstitial cell loss and pancreatitis associated ascites, are still not fully understood. Most studies suggest that the mechanism is related to the exacerbation of mucosal damage caused by pancreatic lesions and the weakening of the ability to resist injury. Pancreatic necrosis, sepsis, Apache 鈪，

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