加用1,6—二磷酸果糖的全肠外营养对严重感染动物及危重病人？…

目的：为比较加用１，６－二磷酸果糖的全肠外营养（ＴＰＮ＋ＦＤＰ）及常规全肠外营养（ＴＰＮ）对危重应激机体的支持效果。 方法：将已造成感染模型的犬分成两组。第一组为ＴＰＮ组（ｎ＝６），输入常规ＴＰＮ液。第二组为ＴＰＮ＋ＦＤＰ组（ｎ＝７），常规ＴＰＮ液加用每天每公斤体重１克ＦＤＰ钠盐。对一组重症应激病人应用１周ＴＰＮ＋ＦＤＰ及常规ＴＰＮ作比较研究，连续５￣７天。 结果：ＴＰＮ＋ＦＤＰ组血、骨骼肌ＡＴＰ     

甘氨酰谷氨酰胺二肽改善猪自体移植小肠的吸收功能

目的：观察甘氨酰谷氨酰胺二肽对猪自体移植小肠吸收功能的作用。方法：杂种猪１０只,行自体小肠移植,术后随机分为两组,标准ＴＰＮ组（ＳＴＰＮ组,ｎ＝５）,接受标准ＴＰＮ支持８天;Ｇｌｙ－Ｇｌｎ二肽组（ＧＴＰＮ组,ｎ＝５）,接受含Ｇｌｙ－Ｇｌｎ的ＴＰＮ支持８天,术后１天（ＰＯＤ１）及术后２８天（ＰＯＤ２８）行木糖吸收实验,测定肠粘膜酶活性。结果：术后２８天,ＧＴＰＮ组：木糖吸收曲线下面积,５ｈ尿液木糖排     

TPN加FDP对严重腹腔感染犬小肠粘膜上皮的保护作用

２０只严重腹腔内感染家犬随机分成三组，即对照组（输入５％ＧＮＳ４ｍｌ·ｋｇ－１／ｈ）、ＴＰＮ组（输入ＴＰＮ液，２９３ｋＪ·ｋｇ－１／ｄ，氮０．５６ｇ·ｋｇ－１／ｄ）及ＴＰＮ＋ＦＤＰ组（除接受ＴＰＮ液外，还接受１，６－二磷酸果糖即ＦＤＰ，１ｇ·ｋｇ－１／ｄ）。营养支持始于感染后６ｈ，止于７２ｈ。ＴＰＮ＋ＦＤＰ组在实验第７２ｈ肠上皮ＤＮＡ，ＲＮＡ含量高于另外两组，肠上皮细胞增殖率亦明显提高（２１％比１３％／ＴＰＮ组，Ｐ＜０．０１；比８％／对照组，Ｐ＜０．０１）。对照组（ｎ＝７）有５只犬于７２ｈ死于感染，ＴＰＮ组（ｎ＝６）３只死亡，而ＴＰＮ＋ＦＤＰ组（ｎ＝７）则仅有２只犬死亡。本研究结果提示，对严重感染犬常规ＴＰＮ加用ＦＤＰ有利于对肠道的保护。     

加用1,6-二磷酸果糖的全肠外营养对严重感染动物及危重病人的支持效果

目的：为比较加用１，６┐二磷酸果糖的全肠外营养（ＴＰＮ＋ＦＤＰ）及常规全肠外营养（ＴＰＮ）对危重应激机体的支持效果。方法：将已造成感染模型的犬分成两组。第一组为ＴＰＮ组（ｎ＝６），输入常规ＴＰＮ液。第二组为ＴＰＮ＋ＦＤＰ组（ｎ＝７），常规ＴＰＮ液加用每天每公斤体重１克ＦＤＰ钠盐。对一组重症应激病人应用１周ＴＰＮ＋ＦＤＰ及常规ＴＰＮ作比较研究，连续５～７天。结果：ＴＰＮ＋ＦＤＰ组血、骨骼肌ＡＴＰ及肌肉磷酸肌酸、细胞色素氧化酶明显高于ＴＰＮ组。给予ＴＰＮ＋ＦＤＰ后，动物２４、４８、７２ｈ血浆ＡＴＰ值明显高于支持前水平（Ｐ＜０．０１）。同时，在２４、４８ｈ时，血浆ＡＴＰ值显著高于ＴＰＮ组（Ｐ＜０．０１）。第２４ｈ骨骼肌ＡＴＰ值（４．７６±０．９７μｍｏｌ／ｇｗｔ）明显高于ＴＰＮ组（３．５４±０．８５μｍｏｌ／ｇｗｔ，Ｐ＜０．０５）。在第２４、４８ｈ时ＣＰ含量明显高于ＴＰＮ组。ＣＣＯ染色颗粒明显增加，经彩色图像分析仪测定第４８ｈ及第７２ｈ骨骼肌ＣＣＯ染色颗粒相对密度值（６．０１±２．０３及６．４５±３．１８）较ＴＰＮ组（３．９７±１．８６及３．１０±１．９２）有明显升高（Ｐ＜０．０１）。结果表明ＴＰＮ＋ＦＤＰ支持组     

1,6—二磷酸果糖对手术后应激病人应用全肠外营养支持效果的影响

本文在胃癌行全胃或胃大部切除术引起的中等程度应激病人，随机分组对比观察了全肠外营养或ＴＰＮ加用１，６－二磷酸果糖的效果。结果显示，与单纯ＴＰＮ相比，ＴＰＮ加用ＦＤＰ后血清皮质醇和胰高血糖素等应激激素水平有所下降，尿中３－甲基组氨酸排出减少，累积氮平衡增加。     

短链脂肪酸对大鼠移植小肠作用的研究

目的：了解短链脂肪酸（ＳＣＦＡ）对大鼠移植小肠萎缩及功能低下是否具有预防作用。方法：近交系Ｗｉｓｔａｒ大鼠行异位全小肠移植后第２天开始给予全肠外营养（ＴＰＮ）至第１０天,对照组（ｎ＝１０）行常规ＴＰＮ支持,ＳＣＦＡ组（ｎ＝１０）行常规ＴＰＮ支持并加用ＳＣＦＡ,观察移植肠形态学及吸收功能。结果：ＳＣＦＡ组移植肠绒毛高度、隐窝深度、粘膜厚度及绒毛面积均明显超过对照组,肠上皮细胞偶见线粒体肿大及部分线粒     

^99mTc—DTPA测定肠道通透性的方法及应用

目的：建立９９ｍ锝┐乙三胺五乙酸（９９ｍＴｃ┐ＤＴＰＡ）测定肠道通透性的方法并观察其在临床和动物实验研究中的应用效果。方法：口服９９ｍＴｃ┐ＤＴＰＡ３７～７４ＭＢｑ，收集２４ｈ尿液，γ计数器测定尿液中ＤＴＰＡ排泄量。采用此方法观察了９例健康人和２５例胃肠道手术病人手术前及术后７天肠道通透性，３组病人术后７天分别给予谷氨酰胺０ｇ／（ｋｇ·ｄ）（Ａ组，ｎ＝８），０．３ｇ／（ｋｇ·ｄ）（Ｂ组，ｎ＝８）和０．６ｇ／（ｋｇ·ｄ）（Ｃ组，ｎ＝９）；１０头杂交猪自体小肠移植后分别给予标准全肠外营养（ＳＴＰＮ组，ｎ＝５）和强化３％甘氨酰谷氨酰胺的全肠外营养（ＧＴＰＮ组，ｎ＝５）２８天观察移植小肠的通透性。结果：９例健康人２４ｈ尿液ＤＴＰＡ排泄率为４．８６±１．８６％，术后７天Ａ、Ｂ二组病人ＤＴＰＡ排泄率较术前明显增加（６．６４±３．９５％ｖｓ１３．７１±４．８５％；８．８８±３．９５％ｖｓ１０．７６±２．８８％，Ｐ＜０．０５），Ｃ组手术前后肠道通透性无变化（６．８０±２．１２％ｖｓ３．５５±１．２９％，Ｐ＞０．０５）。术后２８天ＳＴＰＮ组ＤＴＰＡ排泄率明显高于ＧＴＰＮ组（２４．０１±７．４４％ｖｓ７．７７±３．０４％，Ｐ＜     

短链脂肪酸对TPN大鼠小肠粘膜结构及细胞增殖作用的研究

目的 探讨短链脂肪酸（ＳＣＦＡｓ）对ＴＰＮ大鼠小肠粘膜的保护作用,方法 将３０只近交系Ｗｉｓｔｅｒ（ＲＴ１＾Ｋ）大鼠随机分为假手术对照组,常规ＴＰＮ组及ＳＣＦＡｓ－ＴＰＮ组,进行为期１４天实验,结束后观察小肠粘膜的形态学变化和细胞增殖情况,结果 常规ＴＰＮ组大鼠肠粘膜绒毛高度,宽度及隐窝深产正常对照组均有显著减少,其增殖指数也显著降低,ＳＣＦＡｓ－ＴＰＮ组上述指标明显升高,与对照组基本接近,结论     

全小肠移植术后肠功能的恢复和营养支持

小肠移植是治疗不可逆性肠衰竭的理想方法，合理安排与实施肠内与肠外营养，对移植肠功能的恢复至关重要。手术１－２ｄ后血液动态学平稳，即可开始静脉营养。第３－４天后肠蠕动恢复，即可开始肠道营养，肠道灌注结晶氨基酸类或多肽类要素膳添加谷氨酰胺和中链脂肪酸，有利于肠功能的恢复。完全口服饮食并停止静脉营养，是小肠移植治愈肠衰竭的真正目的。国内首例全小肠移植病人，术后１００ｄ肠功能恢复良好，表现为移植肠消化吸收     

饲料脂肪酸组成对大鼠胃肠等肿瘤生成的影响

目的：　研究脂肪酸组成对甲基亚硝基脲（ Ｍ Ｎ Ｕ） 诱导的大鼠结肠等肿瘤生成的影响。方法：　雄性 Ｓ Ｄ 大鼠喂以用牛油、豆油、紫草油、玉米油和鱼油按不同比例调配，含脂肪量为１５ ％ 的半合成饲料，分５ 组。各组脂肪酸组成为：１ 组以牛油为主富含饱和脂肪酸；２ 组以豆油为主富含亚油酸，１ 组和２ 组基本不含有ｎ ３ 系列多不饱和脂肪酸；３ 组以紫草油为主富含亚油酸，α和γ亚麻酸，ｎ ６／ｎ ３ 脂肪酸之比为４ ．５３ ；４ 组以鱼油为主富含ｎ ３ 系列多不饱和脂肪酸，ｎ ６／ｎ ３ 脂肪酸之比为０ ．７３ ；５ 组为混合油组，ｎ ６／ｎ ３ 脂肪酸之比为１ ．９５ 。对照组和实验组分别经腹腔注射磷酸盐生理盐水缓冲液和３０ ｍｇ／ｋｇ ．ｂｗ 的 Ｍ Ｎ Ｕ，每周一次，共６ 次，喂养１８０ 天。实验期控制了影响肿瘤产生的因素。结果：１ 、２ 和３ 组产生的结肠肿瘤均显著高于４组（ Ｐ＜ ０ ．０５） ，也相对高于５ 组（ Ｐ＞ ０ ．０５） ；１ 、２ 、３ 和５ 组产生的胃肿瘤也相对地高于４ 组，但是，各组之间无显著的统计学差异。除了４ 组和１ 组外，其它各组在其它部位也产生了肿瘤。结论：　 Ｍ Ｎ Ｕ 能诱导喂以不同脂肪酸组成的大鼠产生以结肠癌为主的癌症；饲?     

谷氨酰胺对短肠综合征大鼠残留小肠、结肠形态的影响

目的：观察谷氨酰胺（Gln)对短肠综合征大鼠残留小肠、结肠形态的影响。方法：23只雄性SD大鼠切除80%小肠,随机分为三组：饮食组（n=8)大鼠术后自由进食;全胃肠外营养（TPN）组（n=8)输TPN标准液;Gln组（n=7）输TPN Gln液;正常大鼠8只,作为正常对照组。术后第7天,称体重,取残留空肠、回肠、结肠进行组织学检查（包括光镜和电镜）。结果：饮食组和Gln组术前体重无明显差异,但术后体重有明显差异;饮食组空肠粘膜绒毛高度（VH）和粘膜厚度（MT）、回肠粘膜的VH均明显大于正常组;TPN组空肠粘膜VH、MT明显小于正常组;回肠粘膜隐窝浓度（CD）、MT亦明显小于正常组;Gln组空肠和回肠粘膜VH、CD和MT明显大于TPN组;饮食组结肠MT明显大于正常组,Gln组结肠MT明显大于TPN组。结论：80%小肠切除后,残留小肠发生代偿性改变,食物刺激是残留小肠代偿的重要因素;但这种代偿不完全,TPN可维持机体体重,但可引起残留小肠粘膜萎缩;Gln能阻止TPN引起残留小肠粘膜萎缩,促进残留小肠代偿;同时Gln还促结肠粘膜增生。     

谷氨酰胺对短肠综合征大鼠肝脏及结肠形态的作用

目的：观察谷氨酰胺对短肠综合征大鼠肝脏和结肠形态的影响。方法：23只雄性大鼠切除80％小肠,随机分3组：饮食组8只术后自由进食,全胃肠外营养（TPN）组8只输入TPN标准液,谷氨酰胺（Gln)组7只,输TPN＋Gln,正常大鼠8只,作为对照组。术后第7天,取门静脉血测定肝功能,肝脏和结肠进行组织学检查,结果：饮食组、正常组和Gln组血ALb明显高于TPN组,Gln组血TP明显高于TPN组,光镜下Gln组（2／7）和TPN组（3／8）肝脏标本呈脂肪变性改变,两无显差别,饮食组结肠粘膜厚度明显大于正常组,Gln组结肠粘膜厚度明显大于TPN组。结论：Gln促使结肠粘膜增生,有利于维持血TP和ALb水平,但未能减轻肝脂肪变性。     

Effect of recombinant human growth hormone on the intestinal structure of rats receiving bowel resection and parenteral nutrition

Recombinant human growth hormone (rHGH) can improve nitrogen balance and promotecell proliferation. Little is known about the relationship between rHGH and gastrointestinal mucosal structure and function after bowel resection and parenteral nutrition (PN). The aim of this study was to determine the effect of rHGH on bowel mucosal structure and barrier function in rats receiving 50% small intestinal resection and PN. Thirty Wistar rats with central vein catheterization plus 50% small bowel resection were divided into three groups: chow (chow), standard (STD) and rHGH (rHGH). The chow group received chow food; the STD group was given standard PN; the rHGH group received standard PN plus rHGH (4.8 mg/kg/day, subcutaneously). The groups were maintained on their respective diets for 8 days and then killed. Body weight, small intestinal mucosal thickness, villus height and Goblet cells in the villus were measured. Body weight loss in the STD group was significantly greater than that in the chow and rHGH groups (P< 0.01). The mucosal thickness and villus height of rHGH group were significantly greater than the STD and chow groups (mucosal thickness: 806 +/- 5.5 vs. 533 +/- 6.0 and 593 +/- 6.0 microm; Villus height: 506 +/- 6.0 vs. 295 +/- 5.5 gm and 400 +/- 6.7 lam, respectively) (P< 0.05). The number of Goblet cells in the STD group was significantly greater than the rHGH and chow groups (9.06 +/- 1.07 vs. 5.35 +/- 1.48 and 6.10 +/- 1.51/per villus) (P < 0.01). rHGH can maintain body weight and promote bowel mucosal cell growth and might improve the barrier function of the bowel in rats after 50% small intestinal resection and PN.     

甘氨酰谷氨酰胺二肽改善猪自体移植小肠的组织结构

目的：观察甘氨酰谷氨酰胺（Gly-Gln)二肽对猪自体移植小肠组织结构的作用。方法：杂种猪10只,行自体小肠移植,术后随机分为两组,标准TPN组（STPN组,n=5),接受标准TPN支持28天;Gly-Gln二肽组（GTPN组,n=5)接受含Gly-Gln的TPN支持28天。术后（POD0）及术后28天（POD28）测定肠粘膜谷氨酰胺（Gln)、蛋白质、谷光甘肽过氧化物酶（GSH－PX）活性,肠粘膜图像分析和超微结构观察。结果：术后28天GTPN组;移植小肠Gln、蛋白质、GSH－PX活性、肠绒毛高度、绒毛面积和粘膜厚度显著高于STPN组,肠粘膜超微结构显著优于STPN组。结论：应用Gly-Gln二肽能够显著改善猪自体移植小肠组织结构。     

肠康复治疗对短肠综合征病人残余小肠黏膜形态学的影响

目的:观察重组人生长激素(rhGH)、谷氨酰胺(Gln)和膳食纤维的肠内营养(EN)对短肠综合征病人小肠黏膜形态、肠黏膜细胞增殖和凋亡水平的改变,以评价对短肠综合征病人的治疗效果. 方法:10例短肠综合征病人联合应用rhGH 0.05 mg/(kg·d)、Gln 30 g/d和膳食纤维的EN进行3周的肠康复治疗.分别在...     

添加rhGH与Gln的肠外营养对短肠大鼠代谢效应的影响

目的研究添加人重组生长激素(rhGH)及谷氨酰胺(Gln)的肠外营养(PN)对短肠大鼠机体合成代谢的作用及作用机制. 方法将SD大鼠按2×2析因设计方案随机分成STD、Gln、rhGH及GG 4组,建立PN短肠大鼠动物模型.测定各组大鼠体重及氮平衡变化,测定PN后大鼠各组织器官重量及机体总体水、脂肪及蛋白含量变化,测定血GH及IGF-1浓度. 结果 rhGH组及GG组大鼠体重显著增加,氮平衡改善;腓肠肌重量增加;机体总体蛋白明显升高,体脂下降;血GH及IGF-1显著升高,P值均<0.05;单位长度小肠重量在Gln与rhGH组显著增加,GG组增加最为明显,P<0.05. 结论 rhGH具有显著的促机体合成代谢作用,Gln作用不明显,但二者对残余小肠代偿具有协同促进作用.IGF-1在rhGH的促合成代谢机制中起重要介导作用.     

Comparative effects of glucagon-like peptide-2 (GLP-2), growth hormone (GH), and keratinocyte growth factor (KGF) on markers of gut adaptation after massive small bowel resection in rats

BACKGROUND: Administration of specific growth factors exert gut-trophic effects in animal models of massive small bowel resection (SBR); however, little comparative data are available. Our aim was to compare effects of a human glucagon-like peptide-2 (GLP-2) analog, recombinant growth hormone (GH) and recombinant keratinocyte growth factor (KGF) on jejunal, ileal, and colonic growth and functional indices after 80% SBR in rats. METHODS: Thirty-seven male rats underwent small bowel transection (sham operation) with s.c. saline administration (control; Tx-S; n = 7) or 80% midjejuno-ileal resection (Rx) and treatment with either s.c. saline (Rx-S, n = 7), GLP-2 at 0.2 mg/kg/d (Rx-GLP-2; n = 8), GH at 3.0 mg/kg/d (Rx-GH; n = 8), or KGF at 3.0 mg/kg/d (Rx-KGF; n = 7) for 7 days. All groups were pair-fed to intake of Rx-S rats. Gut mucosal cell growth indices (wet weight, DNA and protein content, villus height, crypt depth, and total mucosal height) were measured. Expression of the cytoprotective trefoil peptide TFF3 was determined by Western blot. Gut mucosal concentrations of the tripeptide glutathione (L-glutamyl-L-cysteinyl-glycine) and glutathione disulfide (GSSG) were measured by high-performance liquid chromatography and the glutathione/GSSG ratio calculated. RESULTS: SBR increased adaptive growth indices in jejunal, ileal, and colonic mucosa. GLP-2 treatment increased jejunal villus height and jejunal total mucosal height compared with effects of resection alone or resection with GH or KGF treatment. Both GH and KGF modestly increased colonic crypt depth after SBR. SBR did not affect small bowel or colonic goblet cell number or TFF3 expression; however, goblet cell number and TFF3 expression in both small bowel and colon were markedly up-regulated by KGF treatment and unaffected by GLP-2 and GH. SBR oxidized the ileal and colonic mucosal glutathione/GSSG redox pools. GLP-2 treatment after SBR increased the glutathione/GSSG ratio in jejunum, whereas KGF had an intermediate effect. In addition, GLP-2 (but not GH or KGF) prevented the SBR-induced oxidation of the glutathione/GSSG pools in both ileum and colon. Conclusions: GLP-2 exerts superior trophic effects on jejunal growth and also improves mucosal glutathione redox status throughout the bowel after massive SBR in rats. Both GH and KGF increase colonic mucosal growth in this model. KGF alone potently increases gut mucosal goblet cell number and expression of the cytoprotective trefoil peptide TFF3. The differential effects of GLP-2, GH and KGF administration in this model of short bowel syndrome suggest that individual therapy with these growth factors may not be an adequate strategy to maximally improve adaptive gut mucosal growth and cytoprotection after massive small intestinal resection. Future research should address the use of these agents in combination in short bowel syndrome.     

Alanyl-glutamine-supplemented parenteral nutrition prevents intestinal ischemia-reperfusion injury in rats

BACKGROUND: Intestinal ischemia-reperfusion (I/R) injury plays an important role in the pathogenesis of systemic inflammation and multiple-organ failure. We studied whether glutamine, the primary fuel of the small intestine, prevents intestinal mucosal damage after intestinal I/R in rats. METHODS: Rats were randomly divided into 4 groups: a sham-standard amino acid (SAA) group (n = 8); a sham-glutamine (Gln) group (n = 8); an I/R-SAA group (n = 10); and an I/R-Gln group (n = 9). Alanyl-glutamine solution was produced by replacing 36% of the total amino acid nitrogen with Gln. The superior mesenteric artery was ligated. After 60 minutes of ischemia, reperfusion was initiated and infusion was started. After 24-hour reperfusion, the intestinal segment was removed for morphological and biochemical analysis, and blood samples were drawn from the portal vein. Fluorescein isothiocyanate-conjugated dextran 70,000 (FITC-dextran) was infused into the duodenum 2 hours before animal death. RESULTS: In the I/R-SAA group, extensive epithelial sloughing and mucosal ulceration of villous tips were observed, whereas these findings did not occur in the I/R-Gln group. Mucosal wet weight, DNA, and protein content decreased significantly in the I/R-SAA group compared with the sham-SAA group and increased significantly in the I/R-Gln group compared with the I/R-SAA group. Plasma FITC-dextran significantly increased in the I/R-SAA group compared with the sham-SAA group, but the plasma level in the I/R-Gln group was comparable with that of each sham group. Mucosal glutaminase activity significantly increased in both the I/R-SAA and I/R-Gln groups compared with the sham-SAA and sham-Gln groups, respectively. CONCLUSIONS: Alanyl-glutamine protects against morphologic and functional mucosal injury after intestinal I/R in rats.     

表皮生长因子增强TPN减少放射性肠炎细菌易位及其机理的实验研究

腹部受辐射 ( abdominal rdiation,AR)致放射性肠炎常导致肠粘膜屏障损害和细菌易位。接受长期 TPN( total parenteral nutrition,TPN)改善营养的同时 ,可加重细菌易位 ,并导致多器官功能衰竭等致死性并发症。即使给予肠粘膜代谢所需的谷氨酰胺 ( Glutamine,Gln)亦不能完全防治其损伤。EGF( epidermal growth factor)是胃肠道粘膜上皮生长和增殖的介质。本研究在 SD大鼠放射性肠炎模型上观察了 EGF增强 TPN对放射性肠炎细菌易位及对损伤的肠粘膜修复的影响 ,结果发现 ,经 EGF增强的 TPN治疗大鼠放射性肠炎 ,大鼠死亡率、细菌易位率均较不用 TPN及应用不含 EGF的 TPN组明显下降 ,体重、粘膜 /肠段重量比、绒毛高度、面积、小肠 Gln摄取率及 DNA含量均明显升高。机理为 :EGF对小肠粘膜有明显的滋养作用。EGF增强 TPN在提供较完善营养及肠道充分休息 ,促进创伤愈合的同时 ,通过提高肠粘膜对 Gln的摄取能力 ,维持肠粘膜上皮的正常代谢 ,加速修复损伤的肠粘膜屏障 ,降低细菌易位率 ,从而降低死亡率