創(chuàng)傷失血性休克論文SPV干預(yù)下重創(chuàng)傷—失血性休克大鼠小腸黏膜病理形態(tài)學(xué)觀察

1、創(chuàng)傷-失血性休克論文：SPV干預(yù)下重度創(chuàng)傷失血性休克大鼠小腸黏膜病理形態(tài)學(xué)觀察【中文摘要】嚴(yán)重創(chuàng)傷后,可引起機(jī)體強(qiáng)烈的應(yīng)激反應(yīng),腸道作為機(jī)體對缺血反映最敏感的器官,腸黏膜屏障損傷導(dǎo)致腸道的通透性增高,造成細(xì)菌及內(nèi)毒素逸出腸腔進(jìn)入腸淋巴管和腸系膜淋巴結(jié),繼而進(jìn)入門靜脈和體循環(huán),引起全身感染和內(nèi)毒素血癥、腸源性膿毒癥、多器官功能障礙綜合癥(MODS)等多種并發(fā)癥。腸道作為外科應(yīng)激的一個中心器官和機(jī)體最大的儲菌庫,如何防治腸道細(xì)菌和毒素移位一直是防治腸源性感染的重要課題。本研究采用能夠引起腸源性感染的重度創(chuàng)傷失血性休克動物模型,通過測定不同時間窗大鼠小腸黏膜病理形態(tài)學(xué)觀察,以探討SPV(Smecta

2、、Polymyxin B、Vitamin B6,簡稱,SPV)對腸黏膜的保護(hù)作用。方法健康雄性SPF級SD大鼠,隨機(jī)分為四組:對照組(n=8),重度休克組(n=40),重度休克復(fù)蘇組(n=40),SPV干預(yù)重度休克復(fù)蘇組(n=40)。后三組依照實(shí)驗(yàn)各時相點(diǎn)分為5個亞組(n=8),大鼠通過股動脈放血、斷股骨和軟組織損傷造成創(chuàng)傷失血性休克大鼠動物模型。重度休克復(fù)蘇組經(jīng)股靜脈回輸血液及林格氏液復(fù)蘇。SPV干預(yù)重度休克復(fù)蘇組在休克模型未復(fù)制前先經(jīng)口-食道向消化道內(nèi)灌注SPV液,休克模型復(fù)制成功后經(jīng)股靜脈回輸血液及林格氏液。各組分別于1h,2h,4h,8h,16h不同時間窗進(jìn)行標(biāo)本取材。統(tǒng)計實(shí)驗(yàn)組間大鼠

3、死亡率,檢測腸黏膜損傷指數(shù),進(jìn)行小腸黏膜形態(tài)學(xué)計量。結(jié)果實(shí)驗(yàn)組間死亡率:與對照組比較,各組實(shí)驗(yàn)大鼠的死亡率具有顯著性差異(P0.05)。腸黏膜損傷指數(shù):與對照組相比,各組各時間窗腸黏膜損傷指數(shù)均顯著增高,差異非常顯著(p<0.01);休克組隨著時間的延長,腸黏膜損傷不斷加劇,各時間窗腸黏膜損傷指數(shù)均顯著增高,差異非常顯著(p<0.01);復(fù)蘇組16h時腸黏膜損傷比1h時有所減輕,差異非常顯著(P<0.01),表明腸黏膜損傷有所恢復(fù);SPV干預(yù)組4h,8h,16h時較1h時腸黏膜損傷程度減輕,差異非常顯著(P<0.01)。與休克組比較,復(fù)蘇組及SPV干預(yù)組,腸黏膜損傷程度

4、均減輕,差異非常顯著(P<0.01);SPV干預(yù)組與復(fù)蘇組相比腸黏膜損傷程度減輕,差異具有顯著性(P<0.05)。腸黏膜絨毛高度:休克組的小腸絨毛高度隨著休克時間的推移逐漸變短,8h,16h腸黏膜變短最嚴(yán)重,差異非常顯著(P<0.01);與休克組相比,復(fù)蘇組和SPV干預(yù)組小腸黏膜絨毛高度水腫,這可能與腸微循環(huán)缺血恢復(fù)血運(yùn)后,腸黏膜逐漸趨于修復(fù)有關(guān),差異非常顯著(P<0.01);SPV干預(yù)組與復(fù)蘇組相比,腸黏膜水腫有所減輕,具有顯著差異(P<0.05)。腸黏膜絨毛厚度:休克組的小腸絨毛厚度隨著休克時間的推移逐漸增粗,差異非常顯著(P<0.01);與休克組相比,

5、復(fù)蘇組和SPV干預(yù)組1h,2h時腸黏膜厚度有所增加,從4h開始逐漸減輕,具有顯著差異(P<0.01);SPV干預(yù)組與復(fù)蘇組相比,有顯著性差異(P<0.05),說明SPV干預(yù)組較復(fù)蘇組恢復(fù)的早且快。結(jié)論(1)重度創(chuàng)傷-失血性休克后隨著時間的推移,腸黏膜廣泛受損,損傷指數(shù)大幅上升,表現(xiàn)為絨毛排列紊亂,乳糜管和血管擴(kuò)張,紅細(xì)胞浸潤或出血,上皮細(xì)胞變性、壞死、與固有層分離、部分脫落、絨毛折斷以至固有層裸露。黏膜肌層水腫、出血、裂解。在修復(fù)過程中,絨毛的高度和厚度恢復(fù),短時間內(nèi)也可能殘存黏膜下和黏膜下肌層的空泡。(2)重度創(chuàng)傷-失血性休克后即使能夠得到液體復(fù)蘇,1h、2h時腸黏膜的損傷也最為

6、明顯,由此說明,腸壁的再灌注性損傷對腸黏膜的損傷力最強(qiáng),而且發(fā)生早。(3)早期口服思密達(dá)+多黏菌素-B+維生素B6混合液,可能具有預(yù)防腸黏膜損害,從源頭上阻斷內(nèi)毒素的釋放和細(xì)菌移位的作用?！居⑽恼縎evere 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 per

7、meability, 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 end

8、otoxin 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.Me

9、thods128 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 t

10、he 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

11、 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 w

12、ere 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 sig

13、nificant (P < 0.05).Intestinal mucosal damage index: Compare with control group, intestinal mucosal damage index increased significantly at all time points of the shock (p<0.01), and there were also significantly differences among the time points in three shock groups (p<0.01). There were l

14、ess damage index at 16h after the shock than those at 1h in resuscitation group (p<0.01). There were less damage index at 4h, 8h,16h after the shock than those at 1h subgroup in SPV intervention group (p<0.01). The structure of intestinal mucosa was less damaged in resuscitation group and SPV

15、intervention group than that in control group (p<0.01), with the lower damage index in SPV intervene group than that in resuscitation group (p<0.05).The height of intestinal mucosa villi: The intestinal mucosa villi was significantly shorted in all shock groups compare with control group (p<

16、;0.01), with the shortest at 8h, 16h after shock. There were severe mucosal edema in resuscitation group and SPV group compared with control group (p<0.01), with less mucosa edema in SPV group than resuscitation group (p<0.05).The thickness of intestinal mucosa villi: Compared with control gro

17、up, the intestinal mucosal villi became thicker in all shock groups at all time points (p<0.01). 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 (p<0.01).

18、There was also significant difference in the thickness of intestinal mucosal villi between SPV group and resuscitation group (p<0.05).Conclusion(1) After severe trauma-hemorrhagic shock,intestinal mucosa is widely damaged with the shock prolonged. The pathological changes include mucosal villi di

19、sarranged, 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 muscul

20、aris 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 after shock, though