摘要
目的探讨严重创伤后肠屏障功能损伤机制及谷氨酰胺(GLN)对肠屏障功能的保护.方法以烧伤、枪伤和缺血再灌流损伤作严重创伤的动物模型,并结合临床病例测定血和组织二胺氧化酶(DAO)活性以及小肠屏障功能的相关指标血乳酸、D-乳酸、肠 PHi,LPS,TNF和尿乳果糖/甘露醇(L/M)的变化,以早期口服 GLN 对肠屏障功能保护.结果严重创伤后血浆 DAO 活性从损伤早期即显著升高,组织 DAO 活性降低,血和小肠组织 DAO 的变化呈负相关(r=-0.937,P<0.001);血浆 DAO 的变化与血浆 TNF,LPS,D-乳酸、乳酸、PHi 和 L/M 的变化呈高度相关(r=0.817,0.842,0.887,0.872,-0.553和0.951,P<0.01~0.05);小肠组织病理变化与功能指标变化一致;早期口服 GLN 可不同程度地改善了肠屏障功能指标.结论严重创伤后肠屏障功能早期即有受损伤;血浆 DAO 活性的变化是反映小肠机械损伤的敏感指标;GLN 对创伤后小肠屏障功能损伤有保护性作用.
AIM To investigate the mechanism of intestinal barrier function injury after severe trauma and protection by glutamine. METHODS Burned patients and animal models of severe trauma replicated by hemorrhagic shock combined with endotoxin infusion and burn injury were observed.Effects of oral glutamine on intestinal barrier function were observed in scalded rats.Various parameters were studied in these experiments as follows:① Plasma levels of diamine oxidase (DAO),tumor necrosis factor (TNF), lipopolysaccharide (LPS) and lactate and D-lactate by biochemical methods;② lactulose/mannitol (L/M) rate in urine by SP-3400;③ pathological examination of intestinal mucosa by LM. RESULTS Plasma DAO activity was significantly increased after injury.There was a negative correlation between plasma DAO and DAO or pHi of intestinal mucosa (r=-0.937,-0.553,P<0.01-0.05).Otherwise,There were all positive correlations between DAO and TNFα, LPS,D-lactate,lactate,L/M,(r=0.817,0.842,0.887, 0.872,and 0.951,P<0.01).Damage of intestinal mucosa was found by pathological examination.Intestinal barrier function was improved in varying degrees after oral glutamine in scalded rat. CONCLUSION Intestinal barrier function was damaged in the early stage,plasma DAO activity may be a sensitive marker of intestinal mechanic injury and GLN may provide protection against intestinal barrier function injury after severe trauma.
出处
《世界华人消化杂志》
CAS
2000年第10期1093-1096,共4页
World Chinese Journal of Digestology
基金
全军"九五"指令性课题(96L053)
关键词
应激障碍
谷氨酰胺
肿瘤坏死因子
肠损伤
intestines/injuries
stress disorders,post-t raumatic
amine oxidase
glutamine
tumor necrosis factor
rats