CAJ | 학술논문

目的研究肠道缺血再灌注损伤时肠淋巴干结扎和ω-3多不饱和脂肪酸(ω-PUFA)对肠道和远隔组织的影响.方法将40只SD大鼠胃造瘘后随机分为假手术组、肠内营养(EN)组、EN+淋巴干结扎(EN+L)组、ω-PUFA组和ω-PUFA+L组5组,每组8只.营养干预7 d后,用动脉夹夹闭肠系膜上动脉60 min,结扎组同时进行肠淋巴干结扎,假手术组只开腹.术后继续原营养干预3 d后,分别测定肠道通透性、肠黏膜形态、细菌培养和血中细胞因子.结果缺血再灌注3 d后,EN组和EN+L组大鼠体重较造瘘前明显下降(P＜0.05),EN+L组大鼠体重明显低于ω-PUFA组和ω-PUFA+L组(P＜0.05).缺血再灌注后第1天,各组大鼠的L/M值均显著增加(P＜0.05或P＜0.01),缺血再灌注后第3天,EN+L组、ω-PUFA组和ω-PUFA+L组大鼠的L/M值均明显低于缺血再灌注后第1天(P＜0.05),EN组和EN+L组大鼠的L/M值明显高于ω-PUFA+L组(P＜0.05);ω-PUFA组和ω-PUFA+L组大鼠的空肠黏膜厚度及绒毛高度均明显高于假手术组、EN组和EN+L组(P＜0.05或P＜0.01),其回肠黏膜厚度及绒毛高度也均明显高于EN组(P均＜0.05);ω-PUFA+L组大鼠的血清内毒素和肿瘤坏死因子-α水平明显低于EN组(P＜0.05),白细胞介素(IL)-6水平明显低于ω-PUFA组(P＜0.05),IL-1β水平明显低于其余各组(P＜0.05);EN组大鼠的肺细胞凋亡指数明显高于其余4组(P＜0.05),其诱导型一氧化氮合酶和髓过氧化物酶浓度明显高于ω-PUFA+L组(P＜0.05),EN+L组大鼠的诱导型一氧化氮合酶浓度也明显高于ω-PUFA+L组(P＜0.05).结论缺血60 min可引起大鼠肠道损伤、肠屏障功能障碍、通透性增加;再灌注72 h后,肠道损伤部分恢复,通透性较缺血后降低,细菌内毒素仍存在移位,肺仍有凋亡细胞.肠淋巴管结扎可弱化肺组织损伤,促进肠黏膜修复,维护肠屏障功能,减少内毒素移位和减轻系统炎症反应.添加ω-3PUFA的EN显著优于普通EN. 目的研究腸道缺血再灌註損傷時腸淋巴榦結扎和ω-3多不飽和脂肪痠(ω-PUFA)對腸道和遠隔組織的影響.方法將40隻SD大鼠胃造瘺後隨機分為假手術組、腸內營養(EN)組、EN+淋巴榦結扎(EN+L)組、ω-PUFA組和ω-PUFA+L組5組,每組8隻.營養榦預7 d後,用動脈夾夾閉腸繫膜上動脈60 min,結扎組同時進行腸淋巴榦結扎,假手術組隻開腹.術後繼續原營養榦預3 d後,分彆測定腸道通透性、腸黏膜形態、細菌培養和血中細胞因子.結果缺血再灌註3 d後,EN組和EN+L組大鼠體重較造瘺前明顯下降(P＜0.05),EN+L組大鼠體重明顯低于ω-PUFA組和ω-PUFA+L組(P＜0.05).缺血再灌註後第1天,各組大鼠的L/M值均顯著增加(P＜0.05或P＜0.01),缺血再灌註後第3天,EN+L組、ω-PUFA組和ω-PUFA+L組大鼠的L/M值均明顯低于缺血再灌註後第1天(P＜0.05),EN組和EN+L組大鼠的L/M值明顯高于ω-PUFA+L組(P＜0.05);ω-PUFA組和ω-PUFA+L組大鼠的空腸黏膜厚度及絨毛高度均明顯高于假手術組、EN組和EN+L組(P＜0.05或P＜0.01),其迴腸黏膜厚度及絨毛高度也均明顯高于EN組(P均＜0.05);ω-PUFA+L組大鼠的血清內毒素和腫瘤壞死因子-α水平明顯低于EN組(P＜0.05),白細胞介素(IL)-6水平明顯低于ω-PUFA組(P＜0.05),IL-1β水平明顯低于其餘各組(P＜0.05);EN組大鼠的肺細胞凋亡指數明顯高于其餘4組(P＜0.05),其誘導型一氧化氮閤酶和髓過氧化物酶濃度明顯高于ω-PUFA+L組(P＜0.05),EN+L組大鼠的誘導型一氧化氮閤酶濃度也明顯高于ω-PUFA+L組(P＜0.05).結論缺血60 min可引起大鼠腸道損傷、腸屏障功能障礙、通透性增加;再灌註72 h後,腸道損傷部分恢複,通透性較缺血後降低,細菌內毒素仍存在移位,肺仍有凋亡細胞.腸淋巴管結扎可弱化肺組織損傷,促進腸黏膜脩複,維護腸屏障功能,減少內毒素移位和減輕繫統炎癥反應.添加ω-3PUFA的EN顯著優于普通EN.
목적 연구장도결혈재관주손상시장림파간결찰화ω-3다불포화지방산(ω-PUFA)대장도화원격조직적영향.방법 장40지SD대서위조루후수궤분위가수술조、장내영양(EN)조、EN+림파간결찰(EN+L)조、ω-PUFA조화ω-PUFA+L조5조,매조8지.영양간예7 d후,용동맥협협폐장계막상동맥60 min,결찰조동시진행장림파간결찰,가수술조지개복.술후계속원영양간예3 d후,분별측정장도통투성、장점막형태、세균배양화혈중세포인자.결과 결혈재관주3 d후,EN조화EN+L조대서체중교조루전명현하강(P＜0.05),EN+L조대서체중명현저우ω-PUFA조화ω-PUFA+L조(P＜0.05).결혈재관주후제1천,각조대서적L/M치균현저증가(P＜0.05혹P＜0.01),결혈재관주후제3천,EN+L조、ω-PUFA조화ω-PUFA+L조대서적L/M치균명현저우결혈재관주후제1천(P＜0.05),EN조화EN+L조대서적L/M치명현고우ω-PUFA+L조(P＜0.05);ω-PUFA조화ω-PUFA+L조대서적공장점막후도급융모고도균명현고우가수술조、EN조화EN+L조(P＜0.05혹P＜0.01),기회장점막후도급융모고도야균명현고우EN조(P균＜0.05);ω-PUFA+L조대서적혈청내독소화종류배사인자-α수평명현저우EN조(P＜0.05),백세포개소(IL)-6수평명현저우ω-PUFA조(P＜0.05),IL-1β수평명현저우기여각조(P＜0.05);EN조대서적폐세포조망지수명현고우기여4조(P＜0.05),기유도형일양화담합매화수과양화물매농도명현고우ω-PUFA+L조(P＜0.05),EN+L조대서적유도형일양화담합매농도야명현고우ω-PUFA+L조(P＜0.05).결론 결혈60 min가인기대서장도손상、장병장공능장애、통투성증가;재관주72 h후,장도손상부분회복,통투성교결혈후강저,세균내독소잉존재이위,폐잉유조망세포.장림파관결찰가약화폐조직손상,촉진장점막수복,유호장병장공능,감소내독소이위화감경계통염증반응.첨가ω-3PUFA적EN현저우우보통EN.
Objective To investigate the effect of intestinal lymphatic duct ligation and ω-3 polyun saturated fatty acids on intestinal and distant organ in intestinal ischemia-reperfusion injury. Methods Totally 40Sprague-Dawley (SD) male rats (SPF grade)after gastrostomy were equally randomized into sham group (Sham), enteral nutrition (EN) group, enteral nutrition and lymphatic duct ligation (EN + L) group, ω-3 polyunsaturated fatty acids (ω-3PUFA) group, and ω-3PUFA and lymphatic duct ligation (ω-3PUFA + L) group. After 7 days of nutritional intervention, rats were subjected to 60 minutes of intestinal ischemia, ischemia plus mesenteric lymph duct ligation, or sham procedures. After 3 days of continuous nutrition intervention using the original nutrient, lymph nodes, lung, intestine, liver, and blood specimens were harvested. Intestinal permeability and morphology, results of bacterial cultures, and serum cytokines were observed or detected. Result After 3 days of intestinal ischemia-reperfusion (I/R), the body weights of rats in EN group significantly decreased when com pared with the pre-I/R levels (P ＜ 0.05), while the body weights of rats in EN + L group were significantly lower than those in ω-PUFA group and ω-PUFA + L group (P ＜ 0. 05). After one day of intestinal ischemia-reperfusion (I/R), the L/M significantly increased in each group (P ＜0.05 or P ＜0. 01). After 3 days of intestinal ischemiareperfusion (I/R) , the L/M were significantly lower than the level one day after ischemia- reperfusion in EN + L group, ω-PUFA group, and ω-PUFA + L group (P ＜ 0.05). The L/M in EN group and EN + L group were significantly higher than that in ω-PUFA + L group (P ＜ 0. 05). The mucosa thickness and villus height of jejunum in ω-PUFA group and ω-PUFA + L group were significantly higher than those in Sham group, EN group, and EN + L group (P ＜ 0. 01 or P ＜ 0. 05). The mucosa thickness and villus height of ileum in ω-PUFA group and ω-PUFA +L group were also significantly higher than those in EN group (P ＜ 0.05). In ω-PUFA + L group, the serum endotoxin level and tumor necrosis factor-α level were significantly lower than those in EN group (P ＜ 0.05), interleukin (IL) -6 level was significantly lower than that in the ω-PUFA group (P ＜ 0.05), and IL-1 β level was significantly lower than those in other groups (P ＜ 0. 05). In EN group, the lung cell apoptosis index was significantly higher than those in other groups (P ＜ 0.05)and the levels of inducible nitric oxide synthase (iNOS)and myeloperoxidase (MPO) were significantly higher than those in ω-PUFA + L group (P ＜ 0. 05). The level of iNOS was also significantly higher in EN + L group than that in ω-PUFA + L group (P ＜ 0.05). Conclusions Sixty minutes of intestinal ischemia can cause intestinal injury, intestinal barrier dysfunction, and increased permeability of intestine. After 72 h of reperfusion, the intestinal injury can be partially recovered and the permeability can be lower than the post-ischemia level; however, bacterial endotoxin translocation and lung apoptotic cells still exist. Intestinal lymphatic ligation can alleviate the lung damage, promote repair of intestinal mucosa, reduce endotoxin translocation, and attenuate the systemic inflammatory response. EN added with ω-3PUFA is remarkably superior to conventional EN.