创伤-失血性休克论文：SPV干预下重度创伤—失血性休克大鼠小肠黏膜病理形态学观察.doc

创伤-失血性休克论文：SPV干预下重度创伤失血性休克大鼠小肠黏膜病理形态学观察【中文摘要】严重创伤后,可引起机体强烈的应激反应,肠道作为机体对缺血反映最敏感的器官,肠黏膜屏障损伤导致肠道的通透性增高,造成细菌及内毒素逸出肠腔进入肠淋巴管和肠系膜淋巴结,继而进入门静脉和体循环,引起全身感染和内毒素血症、肠源性脓毒症、多器官功能障碍综合症(MODS)等多种并发症。肠道作为外科应激的一个中心器官和机体最大的储菌库,如何防治肠道细菌和毒素移位一直是防治肠源性感染的重要课题。本研究采用能够引起肠源性感染的重度创伤失血性休克动物模型,通过测定不同时间窗大鼠小肠黏膜病理形态学观察,以探讨SPV(Smecta、Polymyxin B、Vitamin B6,简称,SPV)对肠黏膜的保护作用。方法健康雄性SPF级SD大鼠,随机分为四组:对照组(n=8),重度休克组(n=40),重度休克复苏组(n=40),SPV干预重度休克复苏组(n=40)。后三组依照实验各时相点分为5个亚组(n=8),大鼠通过股动脉放血、断股骨和软组织损伤造成创伤失血性休克大鼠动物模型。重度休克复苏组经股静脉回输血液及林格氏液复苏。SPV干预重度休克复苏组在休克模型未复制前先经口-食道向消化道内灌注SPV液,休克模型复制成功后经股静脉回输血液及林格氏液。各组分别于1h,2h,4h,8h,16h不同时间窗进行标本取材。统计实验组间大鼠死亡率,检测肠黏膜损伤指数,进行小肠黏膜形态学计量。结果实验组间死亡率:与对照组比较,各组实验大鼠的死亡率具有显著性差异(P0.05)。肠黏膜损伤指数:与对照组相比,各组各时间窗肠黏膜损伤指数均显著增高,差异非常显著(p0.01);休克组随着时间的延长,肠黏膜损伤不断加剧,各时间窗肠黏膜损伤指数均显著增高,差异非常显著(p0.01);复苏组16h时肠黏膜损伤比1h时有所减轻,差异非常显著(P0.01),表明肠黏膜损伤有所恢复;SPV干预组4h,8h,16h时较1h时肠黏膜损伤程度减轻,差异非常显著(P0.01)。与休克组比较,复苏组及SPV干预组,肠黏膜损伤程度均减轻,差异非常显著(P0.01);SPV干预组与复苏组相比肠黏膜损伤程度减轻,差异具有显著性(P0.05)。肠黏膜绒毛高度:休克组的小肠绒毛高度随着休克时间的推移逐渐变短,8h,16h肠黏膜变短最严重,差异非常显著(P0.01);与休克组相比,复苏组和SPV干预组小肠黏膜绒毛高度水肿,这可能与肠微循环缺血恢复血运后,肠黏膜逐渐趋于修复有关,差异非常显著(P0.01);SPV干预组与复苏组相比,肠黏膜水肿有所减轻,具有显著差异(P0.05)。肠黏膜绒毛厚度:休克组的小肠绒毛厚度随着休克时间的推移逐渐增粗,差异非常显著(P0.01);与休克组相比,复苏组和SPV干预组1h,2h时肠黏膜厚度有所增加,从4h开始逐渐减轻,具有显著差异(P0.01);SPV干预组与复苏组相比,有显著性差异(P0.05),说明SPV干预组较复苏组恢复的早且快。结论(1)重度创伤-失血性休克后随着时间的推移,肠黏膜广泛受损,损伤指数大幅上升,表现为绒毛排列紊乱,乳糜管和血管扩张,红细胞浸润或出血,上皮细胞变性、坏死、与固有层分离、部分脱落、绒毛折断以至固有层裸露。黏膜肌层水肿、出血、裂解。在修复过程中,绒毛的高度和厚度恢复,短时间内也可能残存黏膜下和黏膜下肌层的空泡。(2)重度创伤-失血性休克后即使能够得到液体复苏,1h、2h时肠黏膜的损伤也最为明显,由此说明,肠壁的再灌注性损伤对肠黏膜的损伤力最强,而且发生早。(3)早期口服思密达+多黏菌素-B+维生素B6混合液,可能具有预防肠黏膜损害,从源头上阻断内毒素的释放和细菌移位的作用。【英文摘要】Severe trauma may bring about stress response of the body. The intestine is one of the most sensitive organs to ischemic injuries. Dysfunction of intestinal mucosal barrier may increase intestinal permeability, which results in the translocation of bacterial endotoxin from intestinal cavity into lymphatic and vascular systems. Intestine is a surgical stress central organ and the bodys largest bacteria reservoir. Therefore, prevention and treatment of translocation of intestinal bacterial and endotoxin is the key issue on intestinal infection. The study utilized the rat model with severe traumatic-hemorrhagic shock and observed morphological changes of intestinal mucosa at different time points to explore the protective effect of SPV (Smecta, Polymyxin B, Vitamin B6) on intestinal mucosa.Methods128 male Sprague-Dawley(SD) rats (weighting250300g) were randomly divided into 4 groups: control group (n=8); shock group (n=40); resuscitation group (n=40); SPV intervention group (n=40). The last three groups were subdivided into five subgroups (n=8) according to different time points after the shock. The traumatic hemorrhagic shock model was established by arterial bloodletting, femoral fracture and soft tissue injury. The shock resuscitation group was given with the rats own blood and Ringers solution intravenously. SPV intervention group was added with SPV compounds orally before the shock happened. Statistic mortality between experimental rats.Intestinal mucosal damage index were calculated and intestinal mucosal morphologic changes were observed by light microscope.ResultsThe mortality rate of experimental groups: The difference between control group and experimental groups were statistically significant (P 0.05). The difference between shock recovery group、SPV intervention shock recovery group and shock group were statistically significant (P 0.05),but the difference between shock recovery group and SPV intervention shock recovery group were statistically significant (P 0.05).Intestinal mucosal damage index: Compare with control group, intestinal mucosal damage index increased significantly at all time points of the shock (p0.01), and there were also significantly differences among the time points in three shock groups (p0.01). There were less damage index at 16h after the shock than those at 1h in resuscitation group (p0.01). There were less damage index at 4h, 8h,16h after the shock than those at 1h subgroup in SPV intervention group (p0.01). The structure of intestinal mucosa was less damaged in resuscitation group and SPV intervention group than that in control group (p0.01), with the lower damage index in SPV intervene group than that in resuscitation group (p0.05).The height of intestinal mucosa villi: The intestinal mucosa villi was significantly shorted in all shock groups compare with control group (p0.01), with the shortest at 8h, 16h after shock. There were severe mucosal edema in resuscitation group and SPV group compared with control group (p0.01), with less mucosa edema in SPV group than resuscitation group (p0.05).The thickness of intestinal mucosa villi: Compared with control group, the intestinal mucosal villi became thicker in all shock groups at all time points (p0.01). There were less changes of villi thickness in SPV intervention group and resuscitation group than those of shock group at 1h, 2h subgroups, with significantly less changes at 4h subgroup (p0.01). There was also significant difference in the thickness of intestinal mucosal villi between SPV group and resuscitation group (p0.05).Conclusion(1) After severe trauma-hemorrhagic shock,intestinal mucosa is widely damaged with the shock prolonged. The pathological changes include mucosal villi disarranged, lacteals and vessels extended, red blood cell infiltrated or bleeding, degeneration and necrosis of epithelial cells, chyle tubal and vascular dilatation, and lamina propria naked and separated from epithelial layer, or villi broken. There are also edema, hemorrhage and cracking in muscularis mucosa. In the resuscitation process, the height and thickness of mucosal villi may be recovered, but submucosal or submucosal muscularis cavitations may remain for a short period.(2) The damage of intestinal mucosa caused by severe trauma hemorrhagic shock happens obviously at 1h, 2h aft