腹腔高压导致MODS机制尚不十分明确，目前主要研究心、肺、肠道等病理生理改变，但病死率仍高达60%。我们前期研究发现IAH时胆道压力明显升高，提示胆道压力变化可能在IAH致MODS发生中起一定作用。研究表明，急性胆管炎胆道压力升高后胆汁中炎症介质升高；外引流胆汁可改善失血性休克所致脏器变化；TREM-1信号通路触发炎症介质过量释放。因此提出"IAH→胆道高压→TREM-1激活→炎症介质过量释放→MODS"设想，拟用腹腔高压+胆道置"T"管动物模型，探讨胆道压力变化在IAH导致MODS中的作用及可能机制：（1）不同腹腔压力对胆道压力，胆汁、血液中sTREM-1、炎症介质及重要脏器影响；（2）腹腔高压时不同胆道压力状态下胆汁、血液中sTREM-1、炎症介质及重要脏器改变；（3）胆道高压时阻断TREM-1信号通路对胆汁、血液中炎症介质及重要脏器影响。本研究拟为IAH导致MODS的救治提供新思路。

Recent studies have been focusing on the impact of IAH in heart, lung ,kidney, gut etc. However, IAH-induced MODS still carries a high mortality rate up to 60% -70%. It's indicated in our previous study that the pressure of billary tract increases in IAH, which infers that the increase in biliary tract pressure may be significant in the development of IAH-induced MODS. Studies have shown that the inflammatory mediators were released with the elevation of billary tract pressure in acute cholangitis. External biliary drainage can improve organ function in hemorrhagic shock. TREM-1 pathway promotes the secretion of inflammatory mediators, triggers and expands systemic inflammation. Therefore, our hypothesis is "IAH→ biliary tract hypertension →TREM-1 pathway activated →excessive activation of inflammation →MODS". IAH+EBD animal model is introduced to prove our hypothesis from three aspects. First, influences of different intra-abdominal pressure on biliary tract pressure, sTREM-1 level in blood and bile, inflammatory response and organ function. Second, responses of sTREM-1 level, inflammatory response and organ function, when intra-abdominal pressure level keeps steady and biliary pressure level changes. Third, influences of blocking TREM-1 pathway on inflammatory response and organ function in IAH+ high bilitary tract pressure animal model. This topic is expected to inspire new ideas for the treatment of IAH-induced MODS.