摘要
目的:通过应用体外膜氧合技术(ECMO)再灌注猪心脏死亡供体腹腔器官,观察灌注过程中猪肠黏膜屏障功能的变化情况。方法:选取巴马小型猪20头,建立马斯特里赫特(Maastricht)Ⅱ类猪心脏死亡模型,模型成功建立后,于腹主动脉和下腔静脉行ECMO插管,连接ECMO持续运行6 h。在ECMO运行过程中,持续观察猪小肠色泽、弹性及水肿情况,并于基础阶段、判定心脏死亡时、ECMO运行2 h、4 h及6 h时取血液标本检测内毒素、二胺氧化酶(DAO)及肠型脂肪酸结合蛋白(I-FABP);切取猪小肠组织观察病理组织学变化。结果:血清学检测结果示,猪心脏死亡后,各项指标均比基础阶段显著升高(均P<0.05),ECMO运行至2 h时,血清内毒素、DAO和I-FABP分别为(0.305±0.034)EU/mL、(66.28±5.98)U/mL和(22.03±1.38)ng/mL,相比心脏死亡时均有所下降,内毒素和DAO下降更为显著(均P<0.05),I-FABP亦有所下降,但差异无统计学意义(P>0.05),ECMO运行至4 h,血清内毒素、DAO和I-FABP分别为(0.243±0.021)EU/mL、(60.22±5.41)U/mL和(17.86±1.73)ng/mL,与运行ECMO 2 h相比均呈进一步下降趋势(均P<0.05),当ECMO运转至6 h时,血清内毒素、DAO和I-FABP分别为(0.251±0.023)EU/mL、(59.36±8.40)U/mL和(22.48±1.96)ng/mL,相比ECMO运行4 h,血清I-FABP水平明显上升(P<0.05),DAO、内毒素水平无明显差异。病理检查示,猪心脏死亡后,小肠绒毛部分脱落,黏膜腺体排列不规则,大量炎细胞浸润,随着ECMO的运行,肠壁血运逐渐恢复,猪小肠组织病理情况随时间逐渐好转,至ECMO运行4 h时,光镜下可见小肠绒毛偶见脱落,肠黏膜腺体排列大致规则,炎细胞浸润减轻,但ECMO继续运转至6 h时,小肠水肿严重,病理改变较前变差。结论:短期运行ECMO支持技术,对猪心脏死亡后肠黏膜屏障功能具体有一定的保护支持作用,随ECMO运行时间延长,可使肠黏膜屏障功能受到进一步损伤。
Objective:To study the changes of intestinal mucosal barrier during reperfusion of abdominal organs of donation after pig cardiac death by extracorporeal membrane oxygenation(ECMO).Methods:Twenty mini-pigs were used to establish the MaastrichtⅡcardiac death model.After the model was established successfully,abdominal aorta and inferior vena cava were cannulated immediately,then connected to ECMO circuit for six hours.During this procedure,the color,elasticity and edema of small intestine were observed continuously.Blood samples and small intestine tissues were taken at the time of baseline,death announcement,as well as two hours,four hours and six hours after ECMO.At these times,the endotoxin,diamine oxidase(DAO)and intestinal fatty acid binding protein(I-FABP)were detected,pathological changes of the small intestine mucosa were observed.Results:The results of serological test showed that all indicat-ors after cardiac death were significantly higher than those in baseline(all P<0.05).Two hours after ECMO,endotoxin,DAO and I-FABP were(0.305±0.034)EU/mL,(66.28±5.98)U/mL and(22.03±1.38)ng/mL respectively,which were lower than those after cardiac death,endotoxin and DAO decreased more significantly(all P<0.05),I-FABP decreased but the difference was no statistically significant(P>0.05).Four hours after ECMO,endotoxin,DAO and I-FABP were(0.243±0.021)EU/mL,(60.22±5.41)U/mL and(17.86±1.73)ng/mL respectively,which continued a further decline compared with two hours after ECMO(all P<0.05).Six hours after ECMO,endotoxin,DAO and I-FABP were(0.251±0.023)EU/mL,(59.36±8.40)U/mL and(22.48±1.96)ng/mL respectively,and I-FABP was significantly higher than four hours after ECMO(P<0.05),while endotoxin and DAO were no significantly difference.Light microscope indicated that after cardiac death,the villi of the small intestine were shed partially,the mucosal glands were irregular,and a large number of inflammatory cells were infiltrated.While the blood flow to the intestinal wall was gradually restored,the histopathology of the small intestine was also improved during ECMO Four hours after ECMO, the villi of the small intestine were shed occasionally, the intestinal mucosa glands were arranged in a roughly regular, and inflammatory cell infiltration was alleviated. However, six hours after ECMO, the small intestine edema was serious, and pathological changes were worse than before. Conclusion:ECMO shows some degree of protective and supportive effects on the intestinal mucosal barrier function after pig cardiac death in a short time. With the extension of ECMO circuit time, there may be further intestinal mucosal barrier function injury.
作者
马宁
刘蕾
刘懿禾
史源
陈静
张骊
郭庆军
蒋文涛
沈中阳
MA Ning;LIU Lei;LIU Yi-he;SHI Yuan;CHEN Jing;ZHANG Li;GUO Qing-jun;JIANG Wen-tao;SHEN Zhong-yang(First Clinical College,Tianjin Medical University,Tianjin 300192,China;Tianjin First Central Hospital,Tianjin 300192,China)
出处
《天津医科大学学报》
2020年第3期209-212,217,共5页
Journal of Tianjin Medical University
基金
国家自然科学基金资助项目(81870444)
天津市科技计划项目资助(17ZXMFSY00040)
天津市第一中心医院科技基金资助项目(CL29801)。
关键词
体外膜氧合
猪
心脏死亡
肠黏膜屏障功能
extracorporeal membrane oxygenation
pig
cardiac death
intestinal mucosal barrier function
