血小板激活因子在烧伤合并内毒素血症早期肠粘膜损害中的作用

The role of plateletactivating factor in early intestinal mucosal injury after burns combined with endotoxemia

目的：探讨血小板激活因子（ＰＡＦ）在烧伤合并内毒素血症早期肠粘膜损害中的作用。方法：采用２０％ Ⅲ度体表烧伤合并小剂量内毒素（ＬＰＳ１ ｍ ｇ／ｋｇ）注射的大鼠模型，动态检测了肠组织ＰＡＦ、磷脂酶Ａ２（ＰＬＡ２ ）、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含量于致伤后０．５小时显著高于正常对照组，６ 小时达到高峰；肠组织ＸＯ、ＭＤＡ分别与ＰＡＦ呈显著正相关（Ｐ＜ ０．００５ 和Ｐ＜ ０．００１）；在肠组织ＰＡＦ的高峰期，肠粘膜损害更明显。结论：ＰＡＦ在烧伤合并内毒素血症早期肠粘膜损害中起着重要作用；ＸＯ活化、中性粒细胞的浸润及自由基产生是ＰＡＦ导致肠粘膜损害的重要中间机制；肠粘膜固有细胞是ＰＡＦ来源的重要细胞。

Objective:To explore the role of plateletactivating factor (PAF) in early intestinal mucosal injury after burns combined with endotoxemia.Methods:Rats were subjected to a 20% total body surface area Ⅲ degree burns combined with lowdose lipopolysaccharide(LPS) challenge (1 mg/kg),dynamic changes in PAF,phospholipase A 2(PLA 2),xanthine oxidase (XO),melondialdehyde (MDA) in the intestinal tissue were measured.Results:Following burns combined with LPS challenge,intestinal tissue PAF levels increased at 0 5 hour and peaked at 6 hours,which were markedly higher than that of normal controls.Also,intestinal tissue XO and MDA were positively correlated with PAF respectively after burns combined with endotoxemia ( P <0 005 and P <0 001),and intestinal mucosal damage was obvious during the peak phase of PAF.Conclusions:PAF plays an important role in early intestinal mucosal injury via activation of intestinal epithelial XO,production of free radicals,increase in lipoperoxidation and infiltration of neutrophils after burns combined with endotoxemia.Mucosal cells may be the major source of intestinal PAF.