Zhang Xi-ping, Wang Lei, Zhang Jie
Department of General Surgery, Hangzhou First People's Hospital, Hangzhou 310006, China.
J Zhejiang Univ Sci B. 2007 Apr;8(4):228-36. doi: 10.1631/jzus.2007.B0228.
Study on the action mechanism of inflammatory mediators generated by the severe acute pancreatitis (SAP) in multiple organ injury is a hotspot in the surgical field. In clinical practice, the main complicated organ dysfunctions are shock, respiratory failure, renal failure, encephalopathy, with the rate of hepatic diseases being closely next to them. The hepatic injury caused by SAP cannot only aggravate the state of pancreatitis, but also develop into hepatic failure and cause patient death. Its complicated pathogenic mechanism is an obstacle in clinical treatment. Among many pathogenic factors, the changes of vasoactive substances, participation of inflammatory mediators as well as OFR (oxygen free radical), endotoxin, etc. may play important roles in its progression.
重症急性胰腺炎(SAP)所致炎症介质在多器官损伤中的作用机制研究是外科领域的热点。在临床实践中,主要的并发器官功能障碍为休克、呼吸衰竭、肾衰竭、脑病,肝脏疾病的发生率紧随其后。SAP所致肝损伤不仅会加重胰腺炎病情,还会发展为肝衰竭并导致患者死亡。其复杂的发病机制是临床治疗的障碍。在众多致病因素中,血管活性物质的变化、炎症介质以及氧自由基(OFR)、内毒素等的参与可能在其进展中起重要作用。