生长激素对大鼠坏死性胰腺炎肠粘膜屏障损害的治疗作用

目的: 研究生长激素(GH)对急性坏死性胰腺炎(ANP)肠粘膜屏障损害的治疗作用. 方法: 逆行胰胆管注射3.5%牛磺胆酸钠诱导ANP模型.试验分4组,即正常(N)组、假手术(SO)组、坏死(ANP)组和治疗(ANP+GH)组.术后24小时抽血测血浆D-乳酸、血清GH、胰岛素样生长因子(IGF-1)和白蛋白浓度,取末端回肠观察绒毛高度和粘膜厚度变化. 结果: ANP组回肠通透性上升,绒毛高度和粘膜厚度减小,血清白蛋白、GH和IGF-1均下降.GH治疗后ANP鼠肠粘膜病理变化减轻,肠道通透性降低,白蛋白和GH浓度提高,而对血清IGF-1影响不大. 结论: 外源性GH可通过升高血清GH和白蛋白来减轻ANP时肠粘膜屏障的损伤.     

急性坏死性胰腺炎大鼠肠道黏膜屏障功能的损害及肠道细菌移位

目的观察急性坏死性胰腺炎（ANP）时肠道黏膜屏障的变化和肠道细菌移位。方法选择SD大鼠，逆行胰胆管穿刺法诱导制备大鼠ANP模型并分为两组，分别为假手术组（SO）和坏死组（ANP）。术后24h，观察大鼠ANP模型的回肠黏膜通透性、回肠绒毛高度和黏膜厚度的变化，测定血浆D-乳酸浓度和血浆内毒素水平，并行脏器细菌培养。结果ANP组血浆内毒素水平较SO组升高（P〈0．01），细菌培养SO组均无阳性，ANP组细菌培养总阳性率为55．6％，其中以腹水细菌培养阳性率最高，为75．0％，菌种鉴定主要为肠球菌和变形杆菌。ANP组24h后血浆D-乳酸浓度高于SO组，差异有统计学意义（P〈0.01）。ANP组24h回肠黏膜发生病理形态学的改变，从绒毛高度和黏膜厚度测量值上观察发现ANP组肠壁明显变薄。结论本组实验中，大鼠ANP时的回肠黏膜病理形态学的变化提示ANP大鼠肠道的机械屏障明显受损；血浆D-乳酸浓度的显著上升，证明它可从功能上反映ANP大鼠肠道屏障功能的损害。大鼠ANP时的内毒素水平和脏器细菌培养阳性率的升高，证明内毒素血症和肠道细菌移位是由于早期肠道通透性升高和肠道屏障受损所致。     

雷公藤多甙联合生长抑素治疗对大鼠急性坏死性胰腺炎肠道细菌移位的影响

目的 探讨雷公藤多甙联合生长抑素治疗对大鼠急性坏死性胰腺炎(ANP)肠道细菌移位的影响. 方法 逆行胰胆管穿刺注射3.5%牛磺胆酸钠(0.2 ml/100 g)诱导ANP大鼠模型.分为5组:假手术组(SO)、坏死组(ANP)、生长抑素治疗组(ANP+S)、雷公藤多甙治疗组(ANP+T)、雷公藤多甙+生长抑素治疗组(ANP+T+S).术后禁食12 h,不禁水.各组均随机标记6只观察术后生存时间.术后24h,观察血清淀粉酶、血清脂肪酶活性,血浆内毒素水平,脏器细菌培养结果,胰腺和回肠黏膜病理学变化及大鼠存活率. 结果 雷公藤多甙与生长抑素联合治疗ANP大鼠,可以显著降低血清淀粉酶、血清脂肪酶活性;减轻胰腺组织和肠黏膜炎症细胞浸润、水肿;降低血浆内毒素水平和脏器细菌培养阳性率;提高ANP大鼠存活率. 结论 ANP大鼠存在肠道细菌移位;雷公藤多甙联合生长抑素的治疗可减轻ANP大鼠胰腺和肠道损伤,加强肠道的生物学屏障,降低肠源性细菌及内毒素移位发生率,阻止ANP的发展.     

生长激素对肝大部切除术后鼠肠黏膜的保护作用

目的: 探讨鼠肝大部切除术后生长激素对肠黏膜屏障的保护作用,为临床使用重组人生长激素保护肠黏膜提供实验依据.方法: 90只SD大鼠随机分为对照组、生理盐水(normal saline,NS)组和生长激素(recombinant human growth hormone,rhGH)组,后两组切除肝左叶和右叶;各组连续用药6 d,分别于术后第1,2,3,5和10天取回肠组织行光镜形态学观察及图像分析检测肠黏膜厚度和绒毛高度,并对回肠黏膜上皮细胞行核增殖抗原(proliferate cell nucleus antigen,PCNA)免疫组织化学测定;取心脏血4~6 ml,检测内毒素.结果: 肝大部分切除术后第1,2天,内毒素明显升高,而rhGH组与对照组无明显差异.术后第3,5天,回肠黏膜明显萎缩,绒毛变薄;黏膜上皮细胞PCNA明显下降(P<0.01).应用rhGH 3 d后,回肠绒毛高度、黏膜厚度和PCNA度均增加(P<0.01);术后第5天,达到对照组水平.结论: 肝大部分切除术后肠黏膜屏障受损,应用rhGH可保护肠黏膜屏障,减少血浆内毒素水平.     

枳术汤加味对大鼠肠黏膜屏障功能的保护作用

目的 探讨中药枳术汤加味对大鼠肠黏膜屏障功能的保护作用及其机制.方法 将70只雄性大白鼠随机分为对照组(10只)、造模组(20只)术前连续7d饮水灌胃0.35ml/次,每天2次,治疗组(20只)术前连续7d中药灌胃0.35ml/次,每天2次,大剂量治疗组(20只)术前连续7d中药灌胃0.7ml/次,每天2次.大鼠按2.5ml/kg体重的剂量给予腹腔内注射5%水合氯醛进行麻醉.进腹后血管钳夹闭肠系膜上动脉,持续30min后恢复血供,使肠道发生缺血-再灌注损伤.分别在再灌注1、24h后进行以下检测:肠道细菌移位发生率;回肠黏膜病理变化;外周血浆D-乳酸浓度、二胺氧化酶浓度;回肠黏膜细胞凋亡指数.结果 缺血-再灌注1、24h后细菌移位阳性率、细菌培养阳性率和血浆D-乳酸和二胺氧化酶浓度,造模组高于对照组(P<0.05);治疗组低于造模组(P<0.05);大剂量治疗组和治疗组比较差异无统计学意义(P>0.05). 回肠膜黏重量、绒毛高度及宽度,造模组小于对照组(P<0.05);治疗组大于造模组(P<0.05);大剂量治疗组和治疗组比较差异无统计学意义.肠黏膜上皮细胞凋亡指数,造模组高于对照组(P<0.05);治疗组低于造模组(P<0.05);大剂量治疗组和治疗组比较差异无统计学意义(P>0.05). 结论中药枳术汤加味能减少肠道细菌移位,降低肠黏膜的通透性,可以保护肠黏膜屏障功能.     

重组生长激素对肾病综合征大鼠血清蛋白的影响

目的:观察基因重组生长激素(rhGH)对肾病综合征大鼠(NS大鼠)血清总蛋白、白蛋白和胰岛素样生长因子-1(IGF-1)的作用.方法:制备阿霉素大鼠NS模型,设正常组(6只)、模型组 (12只)和rhGH治疗组 (12只).以放射免疫法(RIA)测血清IGF-1水平,用酶联免疫吸附试验测尿微量白蛋白浓度(Alb),S-丽春红测 24 h尿蛋白定量,全自动生化仪测量血清总蛋白和白蛋白.结果:模型组大鼠血清蛋白、血清IGF-1浓度均显著低于正常组.rhGH治疗4周时血清IGF-1和血清蛋白与模型组大鼠同期相比显著上升;而rhGH治疗组与模型组同期尿蛋白排出无统计学差异.结论:NS时,尿蛋白排出量增加和血清GH/IGF-1轴紊乱导致血清蛋白水平下降,外源性rhGH在不增加尿蛋白排出的情况下可提高NS血清IGF-1和蛋白水平.     

不同营养方式对肠道缺血再灌注大鼠肠屏障功能的影响

目的探讨不同营养物质及支持途径对肠道缺血再灌注大鼠肠屏障功能和细菌易位的影响。方法60只雄性SD大鼠建立肠道缺血再灌注模型,随机分成普通肠外营养组(PN),富含谷氨酰胺的肠外营养组(G-PN),普通肠内营养组(EN)及免疫增强型肠内营养组(IEN)。从术后第1天起连续营养支持7d,各组等氮、等热卡。观察肠道形态学、肠道黏膜通透性、肠道细菌易位情况和血浆内毒素水平及肠道免疫功能检测。结果PN组肠黏膜明显萎缩,其绒毛高度、黏膜厚度、隐窝深度及绒毛表面积均显著低于其他各组(P<0.05);其肠黏膜通透性及内毒素值显著高于其他各组(P<0.05),细菌易位率(100%)明显高于其他各组(G-PN组60.0%,EN组33.3%,IEN组20.0%)。PN组CD4 T淋巴细胞和IgA 浆细胞分布显著低于其他各组(P<0.01)。结论EN在维护肠黏膜屏障功能、防止细菌及内毒素易位方面优于PN。免疫增强型EN在维护肠黏膜屏障、改善肠道免疫功能、防止细菌易位方面作用优于普通EN。     

参附汤预先给药对内毒素血症大鼠肠黏膜屏障功能的影响

目的 评价参附汤预先给药对内毒素血症大鼠肠黏膜屏障功能的影响.方法 选择健康成年雄性SD大鼠24只,4～6月龄,体重180～220 g.采用随机数字表法,将其分为3组(n=8):正常对照组(C组)、内毒素血症组(E组)和参附汤预先给药组(S组).采用尾静脉注射脂多糖(LPS) 10mg/kg建立内毒素血症模型.建模前30 min,E组和S组分别腹腔注射生理盐水和参附汤5ml/kg.于建模后2h时取腹主动脉血样,采用ELISA法检测血浆TNF-α、IL-6、肠-脂肪酸结合蛋白(i-FABP)和D-乳酸(D-lac)浓度;取远端回肠,采用免疫组化法检测肠黏膜上皮细胞间紧密连接蛋白(ZO-1)表达,HE染色,光镜下观察肠黏膜病理学结果,并行Chiu评分.结果 与C组比较,E组和S组血浆TNF-α、IL-6、i-FABP和D-lac浓度升高,肠黏膜Chiu评分升高,肠黏膜上皮细胞间ZO-1表达下调(P＜0.05).与E组比较,S组血浆TNF-α、IL-6、i-FABP和D-lac浓度降低,肠黏膜Chiu评分降低,肠黏膜上皮细胞间ZO-1表达上调(P＜0.05).结论 参附汤预先给药可减轻内毒索血症大鼠肠黏膜损伤,保护肠黏膜屏障功能,其机制与抑制全身炎性反应有关.     

谷氨酰胺和生长激素对门静脉高压症术后营养状态和肠黏膜屏障的影响

目的 观察谷氨酰胺和生长激素联合肠外营养对肝硬化门静脉高压症手术患者术后营养状态和肠黏膜屏障的影响.方法 选择58例接受门静脉高压症手术的肝硬化患者,随机分为两组:实验组(添加谷氨酰胺和重组人生长激素,n=30)和标准营养组(对照组,n=28),两组术后第3天开始进行等氮等热量(每天125kJ/kg体重)营养支持,持续7d.术前、术后第3和第10天清晨分别抽取静脉血检测血清前白蛋白、转铁蛋白,并对手术前、后的尿乳果糖/甘露醇排泄率比值(L/M)、十二指肠黏膜绒毛高度、陷窝深度及肠黏膜增殖细胞核抗原(PCNA)指数进行对比.结果 实验组在术后第10天血清前白蛋白:(199.81±8.77)mg/L、转铁蛋白:(2.28±0.19)mg/L均显著高于对照组(P<0.05),L/M值升高小于对照组(P<0.05),肠黏膜绒毛高度(375.15±23.64)μm和陷窝深度(128.53±16.42)μm均大于对照组(P<0.05)及术前(P<0.05),肠黏膜上皮PCNA指数(24.27±4.25)大于对照组(P<0.05). 结论谷氨酰胺和生长激素联合肠外营养能够改善门静脉高压症手术后营养状态,降低小肠黏膜通透性,并维护肠黏膜形态学完整性,作用优于标准胃肠外营养.     

帕瑞昔布钠对脓毒症小鼠肠黏膜屏障的保护作用

目的研究帕瑞昔布钠对脓毒症小鼠肠黏膜屏障功能的影响及可能机制。方法 21只C57BL/6小鼠随机分为三组:假手术组(Sham组)、脓毒症模型组(CLP组)、脓毒症模型+帕瑞昔布钠2mg/kg治疗组(P组),每组7只。术后24h用襻环结扎法检测各组小鼠小肠通透性。另21只C57BL/6小鼠随机分为三组,分组及治疗同前,术后24h处死小鼠,收集小鼠回肠。小肠组织行HE染色观察肠病理损伤。采用Western bolt法检测小肠ZO-1、Occludin、Claudin-1等紧密连接蛋白的表达。采用ELISA法检测小肠黏膜IL-6、PGE2的浓度。结果与Sham组比较,CLP组小鼠小肠明显损伤,门静脉血内FD4浓度明显升高,小肠黏膜内ZO-1、Occludin、Claudin-1蛋白表达明显减少、IL-6与PGE2浓度明显升高(P0.05)。与CLP组比较,P组小鼠小肠损伤明显减轻(P0.05),门静脉血内FD4浓度明显降低(P0.05),小肠黏膜内各蛋白表达水平明显增加、IL-6与PGE2浓度明显降低(P0.05)。结论帕瑞昔布钠治疗可以明显降低脓毒症导致的肠黏膜屏障功能损伤,其机制可能与降低肠组织炎症水平,增加肠紧密连接蛋白表达相关。     

Reversal of the effect of albumin on gut barrier function in burn by the inhibition of inducible isoform of nitric oxide synthase

HYPOTHESIS: The use of albumin in the early resuscitation formula after major burn has been forbidden because of its damaging effect on the gut barrier function. We hypothesize that inhibition of the inducible isoform of nitric oxide synthase to stabilize endothelial permeability and to retain albumin in the vascular space will ameliorate the major trauma-induced gut barrier dysfunction. DESIGN, INTERVENTIONS, AND MAIN OUTCOME MEASURES: In experiment 1, specific pathogen-free rats undergoing 35% total body surface area burn or sham burn were given equal volumes (7.5 mL/kg) of isotonic sodium chloride solution or albumin from femoral veins for fluid resuscitation at 0, 4, or 8 hours after burn. In experiment 2, intraperitoneal S-methylisothiourea sulfate (7.5 mg/kg) was given immediately after burn to rats from different groups, as in experiment 1 (SMT groups). At 24 hours after burn, the intestinal mucosa was assayed for myeloperoxidase activity as an index for neutrophil sequestration, the distribution of fluorescein isothiocyanate-dextran across the lumen of small intestine was determined to evaluate the intestinal permeability, and bacterial translocation (BT) to the mesenteric lymph nodes (MLNs) and histological findings in the ileum were also examined. RESULTS: Compared with sham burn, burn induced significant increases in intestinal mucosa myeloperoxidase activity, intestinal permeability, BT to the MLNs, and villi sloughing in rats. Albumin administration at 0 or 4 hours after burn enhanced the increases in neutrophil sequestration, permeability, and villi sloughing compared with saline injection at the same times. In contrast, injection of albumin in the burn-SMT group did not aggravate these changes in intestinal myeloperoxidase activity, intestinal permeability, BT to the MLNs, and villi edema. Burn-SMT rats with albumin injections at 4 or 8 hours after burn showed significant 35% and 52% decreases, respectively, in intestinal permeability compared with burn-SMT-saline rats. Use of albumin at 8 hours after burn in combination with S-methylisothiourea significantly attenuated BT to the MLNs and reduced villi edema. CONCLUSIONS: Early albumin resuscitation aggravated the burn-induced gut damage. Albumin administration and inhibition of the inducible isoform of nitric oxide synthase in combination decreased burn-induced gut barrier dysfunction and reversed the damaging effect of albumin on gut barrier function and decreased BT.     

能全素对5-FU化疗后大鼠肠屏障功能的影响

目的 研究评价肠内营养对5-FU化疗后大鼠肠屏障功能的影响.方法 30只SD大鼠被随机分为3组:EN组:单纯能全素肠内营养;STD组:5-FU化疗+能全素肠内营养;CHOW组:腹腔注射5-FU化疗+自由进食.化疗前后观察各组大鼠体重、尿乳果糖/甘露醇的变化,并在第8 d时测定门静脉血内毒素水平、门静脉血和淋巴结培养以及取结肠、回肠标本进行组织学病理切片,测定绒毛高度和肠壁厚度.结果 和EN组相比,STD组大鼠体重明显下降、尿乳果糖/甘露醇比值增加,黏膜高度和肠壁厚度也明显降低;EN组大鼠体重、尿乳果糖/甘露醇等各项观察指标略差于CHOW组.结论 5-Fu可引起大鼠肠屏障损害;单纯能全素肠内营养对化疗后大鼠肠屏障的保护作用不如自由进食.     

急性坏死性胰腺炎并发感染的机理研究

目的观察急性坏死性胰腺炎时肠屏障损伤与细菌移位情况,探讨急性胰腺炎继发感染的机理。方法１５只犬于肠道内定植ＰＵＣ１８质粒菌ＪＭ１０９后,分对照组（ｎ＝７）和急性坏死性胰腺炎组（ＡＮＰ,ｎ＝８）。ＡＮＰ组经主胰管注入牛磺胆酸钠和胰蛋白酶制作ＡＮＰ模型。结果ＡＮＰ组较对照组血胰淀粉酶显著升高（Ｐ＜０．０１）;尿中乳果糖／甘露醇比值高出对照组２～１２倍;空、回、盲肠粘膜及肠内容物中大肠杆菌明显增加（Ｐ＜０．０１）,双歧杆菌、乳酸杆菌明显减少（Ｐ＜０．０１、Ｐ＜０．０５）。对照组犬血培养阴性,除２只犬肠系膜淋巴结培养出细菌外,其余脏器培养均阴性。ＡＮＰ组犬血和脏器细菌培养阳性率均为１００％,且每只犬都能检出术前定植于肠道的质粒菌ＪＭ１０９;胰腺腺泡出血、坏死;肠粘膜绒毛破坏;血浆、回肠组织二胺氧化酶活性下降。结论ＡＮＰ时肠粘膜屏障功能严重受损,发生肠道细菌移位,成为继发性胰腺感染的潜在根源。     

Relationship between disruption of the unstirred mucus layer and intestinal restitution in loss of gut barrier function after trauma hemorrhagic shock

BACKGROUND: The factors involved in shock-induced loss of gut barrier function remain to be defined fully and studies investigating gut injury have focused primarily on the systemic side of the intestine. METHODS: Male Sprague-Dawley rats were subjected to a laparotomy (trauma) and 90 minutes of trauma sham shock (T/SS) or actual trauma (laparotomy) hemorrhagic shock (T/HS) (30 mm Hg). At 0, 30, 60, or 180 minutes after the end of shock and volume resuscitation (reperfusion), the animals were killed and samples of the ileum were collected for intestinal morphologic analysis, analysis of the unstirred mucus layer, and for barrier function by measuring permeability to flourescein dextran. RESULTS: T/HS-induced morphologic evidence of mucosal injury as well as epithelial apoptosis was present at the end of the shock period and maximal after 60 minutes of reperfusion. At 3 hours after reperfusion, the degree of villous injury and enterocyte apoptosis had decreased. In contrast to the morphologic appearance of the villi, disruption of the mucus layer became progressively more severe over time and was manifest as a decrease in mucus thickness, progressive loss of coverage of the luminal surface by the mucus layer, and a change in mucus appearance from a dense to a loose structure. Studies of intestinal permeability documented that T/HS-induced loss of gut barrier function persisted throughout the 3-hour reperfusion period and were associated with injury to the mucus layer as well as the villi. CONCLUSIONS: T/HS leads to changes in the intestinal mucus layer as well as increased villous injury, apoptosis, and gut permeability. Additionally, increased gut permeability was associated with loss of the intestinal mucus layer suggesting that T/HS-induced injury to the mucus layer may contribute to the loss of gut barrier function.     

胰岛素样生长因子Ⅰ在生长激素促小肠代偿中的作用

目的　探讨胰岛素样生长因子Ⅰ（insulin-like growth factorⅠ,IGFⅠ）在生长激素（growthhormone,GH）促小肠代偿中的作用。　方法　将20只SD大鼠随机分成GH组及STD组,建立PN短肠大鼠动物模型。用光镜检查小肠粘膜形态学变化,用放射性免疫分析法测定血GH及IGFⅠ浓度,用Northernblot法测定残存小肠IGFⅠmRNA表达。结果　GH组大鼠小肠粘膜厚度、绒毛高度及隐窝深度均显著高于STD组,分别为(471±16)μmvs.(374±13)μm,(299±17)μmvs.(212±19)μm及(161±20)μmvs.(96±9)μm,P＜0.01。血GH及IGFⅠ浓度在GH组显著高于STD组,分别为(5.2±0.8)ng/mlvs.(3.3±1.7)ng/ml及(425±19)ng/mlvs.(326±30)ng/ml,P＜0.05,残存小肠形态学改变与血GH及IGFⅠ浓度变化间呈显著正相关。GH组小肠局部IGFⅠmRNA的表达显著高于STD组(0.62±0.04vs.0.41±0.02),P＜0.05。结论IGFⅠ在GH的促小肠代偿机制中起着重要的介导作用,全身性IGFⅠ增加及小肠局部IGFⅠ产生的增加均与小肠的代偿密切相关。     

急性坏死性胰腺炎并发感染防治方法的实验研究

目的 观察不同方法对急性坏死性胰腺炎（ＡＮＰ）并发感染的防治效果。方法 用胰管逆行注入法复制犬和大鼠ＡＮＰ模型,将大鼠随机分为非治疗组和中药、微生态、导泻、选择性肠道脱污染（ＳＤＤ）和生长抑素５个治疗组,观察胰、肠组织学、肠上皮细胞间连接结构、肠通透性、肠道菌群、脏器细菌移位率和病死率的变化。结果 中药清胰汤、双歧杆菌合剂和ＳＤＤ能明显改善肠道屏障的肠通透性,减轻细菌移位,降低病死率,单纯导泻效果     

HMGB1 mRNA表达对急性坏死性胰腺炎大鼠肠黏膜ZO-1 mRNA及其蛋白表达的影响

目的研究高迁移率族蛋白B1（high mobility group box-1 protein,HMGB1）mRNA表达对急性坏死性胰腺炎（acute necrotizing pancreatitis,ANP）大鼠肠黏膜紧密连接蛋白-1（zonula occludens protein-1,ZO-1）表达的影响,初步探讨ANP时肠黏膜屏障损伤的可能机理。方法将96只Wistar大鼠随机（随机数字表法）均分为ANP组、丙酮酸乙酯（EP）组及假手术组,3组均分别于术后6、12、24及48 h时各抽取8只大鼠,取腹主动脉血和回肠组织。采用全自动生化分析仪检测血淀粉酶（AMY）水平,采用改良酶学分光光度法检测血浆D-乳酸水平,采用硫代巴比妥酸（TAB）比色法检测回肠组织丙二醛（MDA）含量,采用HE染色法观察大鼠回肠组织的病理学改变,采用免疫组织化学法（SP法）观察回肠组织ZO-1蛋白的表达,采用逆转录聚合酶链反应（RT-PCR）法检测回肠组织HMGB1和ZO-1 mRNA的表达。结果各时相EP组大鼠的血AMY、D-乳酸和回肠组织MDA含量均低于ANP组（P〈0.05）。6 h时,ANP组大鼠回肠组织HMGB1 mRNA的表达即上调,但ZO-1 mRNA的表达下调;各时相EP组大鼠回肠组织HMGB1 mRNA的表达水平均低于ANP组,但ZO-1 mRNA的表达水平均高于ANP组（P〈0.05）。各时相EP组大鼠回肠组织的病理学损伤均较ANP组明显减轻。结论 ANP大鼠回肠黏膜组织中ZO-1表达下调是ANP大鼠肠黏膜屏障损伤的重要原因之一,可能与炎症介质HMGB1的过度表达有关。     

Mucosal hyperplasia of the ileum after subtotal colectomy in rats

To evaluate factors contributing to ileal mucosal hyperplasia following extensive colectomy, the following three models were designed in rats: Subtotal colectomy and end-to-end ileoproctostomy; retransection of the terminal ileum with end-to-side proximal-ileoproctostomy (colectomy group), End-to-side ileoproctostomy without colectomy (bypass group), and End-to-side ileocecostomy (control group). In all groups the terminal ileum was left out of the intestinal stream as defunctionalized segments. Specimens were obtained from the terminal ileum during operation and from both the functioning and the defunctionalized segments at various intervals postoperatively. The mucosal hyperplasia was evaluated by measuring eight variables including numbers of villi around the bowel circumference, villous height, crypt depth, total mucosal thickness, epithelial cell counts per villus, DNA contents per unit length of the bowel and radioactivity of incorporated 3H-thymidine as well as DNA specific activity. The results showed that marked mucosal hyperplasia of the functioning segments was noted in all groups, and that mucosal hyperplasia was also observed in defunctionalized segments of colectomized rats, but not in those of both bypass rats and control. These findings were statistically confirmed by analysis of variance. It was concluded that although intraluminal factors played an important role in mucosal hyperplasia of the ileum following extensive colectomy, humoral factors might be also involved in intestinal adaptation.