烧伤合并内毒素血症早期肠粘膜损害机制的研究

目的：探讨烧伤合并内毒素血症早期肠粘膜损害的发生机制。方法：采用２０％Ⅲ度体表烧伤合并小剂量内毒素（ＬＰＳⅠｍｇ／ｋｇ）注射的大鼠模型，动脉检测了肠组织血小板激活因子（ＰＡＦ）、黄嘌呤氧化酶（ＸＯ）、丙二醛（ＭＤＡ）等的变化。结果：烧伤合并内毒素注射后肠组织ＰＡＦ升高较ＸＯ则，０．５-ｈ即显著高于正常对照组，６ｈ达高峰 ，肠组织ＸＯ和ＭＤＡ分别与ＰＡＦ呈显著正相关（Ｐ〈０．００５；Ｐ〈０．００１），

A study on mechanism of early intestinal mucosal damage after burns combined with endotoxemia in rats

Objective: To explore the mechanism of early intestinal mucosal damage after burns combined with endotoxemia in rats Methods: After the rats were inflicted with 20%TBSA full thickness skin burns and injected with LPS at a dosage of 1 mg/kg B M The dynamic changes of platelet activating factor (PAF), xanthine oxidase (XO) and melondialdehyde (MDA) in the intestinal tissue were observed Results: The increase of PAF level in the intestinal tissue in burns combined with endoxin group (BCEG) was earlier than that of XO level, and its level was higher than that in normal control group (NCG) at the 0 5th h and peaked at the 6th h after burns Both XO activity and MDA content in the intestinal tissue were positively correlated with PAF level respectively(P< 0 001 and 0 005) Meanwhile, the former 2 parameters were also positively correlated with each other (P< 0 01) During the peak phase of PAF and MDA, intestinal mucosal damage was most evident Conclusion: The early intestinal mucosal damage is due to activation of intestinal epithelial XO and macrophages and production of free radicals induced by release of PAF and other inflammatory mediators Together with the infiltration of neutrophils, all of these results in the intestinal mucosal damage after burns combined with endotoxemia