一氧化氮在梗阻性黄疸大鼠肝、肾、肠组织中含量变化及意义

目的 了解一氧化氮（NO）在梗阻性黄疸大鼠肝，肾，肠组织中含量变化及意义。方法 大鼠胆总管结扎后，分别于第一周内和第三周内变化Aminoguanidine(AG)抑制NO合成，同时应用生理盐水（NS）作对照，检测不同时段抑制NO合成后大鼠肝，肾，肠组织中NO和丙二醛（MDA）含量，肌酐清除率（Ccr)，血清总胆红素（T－BIL）和丙氨酸氨基转移酶（ALT）含量及肠系膜淋巴结细菌移位（BT）率的变化。结果 胆总管结扎后，大鼠肝，肾，肠组织中NO含量明显升高，在胆总管结扎第一周抑制NO合成后，肝，肾肠组织中NO含量明显下降，MDA含量明显升高，血ALT明显升高，Ccr明显下降，肠系膜淋巴结BT率明显升高；而在胆总管结扎第三周抑制NO合成后，肝，肾，肠组织中NO和MDA含量明显下降，血ALT明显下降，Ccr明显升高，肠系膜淋巴结BT率明显下降。结论 NO在胆道梗阻引起的肝，肾，肠粘膜屏蔽功能障碍的发生机制中具有重要作用，既有保护作用，又有损害作用。梗阻早期表现为对组织的保护作用，后期表现为对组织的损害作用。     

阻塞性黄疸时L-精氨酸对肾功能的保护作用

目的：研究阻塞性黄疸（OJ）时，L－精氨酸（L－Arg)对肾功能的保护作用。方法：胆总管结扎大鼠30只，随机分成生理盐水对照（NS）组、L－精氨酸（L－Arg)组和L－硝基精氨酸（L－NNA）组，每组10只。胆总管结扎后第2天起分别腹腔注射1ml NS、1ml L-Arg(500mg/kg)、1ml L-NNA(10mg/kg)，连用9d；假手术（SO）组用1ml NS腹腔注射。观察各组肾功能的变化，同时测定血和肾组织内皮素（ET）、一氧化氮（NO）水平、一氧化氮合酶（NOS）活性和丙二醛（MDA）的含量。并用图像分析检测ET1 mRNA和NOS mRNA表达的部位及量的变化。结果：用L－Arg后，血和肾组织NOS活性增加，肾组织ET1 mRNA表达减少，血和肾组织ET下降，NO升高；同时伴有内生肌酐清除率（Ccr)、肾皮质平均血流（RCBF）的升高，肾组织MDA含量降低。结论：L－Arg通过增强血和肾组织NOS活性来增加体内NO水平、抑制ET1 mRNA表达、降低体内ET水平，从而提高Ccr与RCBF，减轻阻塞性黄疸时的肾功能损伤。     

褪黑素对梗阻性黄疸大鼠肝损伤保护作用的实验研究

目的探讨氧化性损伤在大鼠梗阻性黄疸肝功能损害发生中的作用以及褪黑素对其的保护作用。方法成年雄性SD大鼠64只,采用完全随机化法随机分为正常对照组（CN组,n=16）、假手术组（SO组,n=16）、胆总管结扎组（BDL组,n=16）和胆总管结扎＋褪黑素治疗组（BDL＋MT组,n=16）。应用胆总管结扎法建立梗阻性黄疸模型,褪黑素治疗组大鼠手术前1 d至手术后7 d连续腹腔注射褪黑素0.5 mg（/kg.d）,每日10∶00给药。分别于手术后第4 d和第8 d两个时间点采集标本,检测血浆中总胆红素（TBIL）、丙氨酸转氨酶（ALT）、门冬氨酸转氨酶（AST）、碱性磷酸酶（AKP）及γ-谷氨酰转肽酶（GGT）水平变化,比色法测定肝组织匀浆中丙二醛（MDA）、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽（GSH）、谷胱甘肽过氧化物酶（GSH-Px）含量或活力变化,采用TUNEL法检测肝组织细胞凋亡,并计算肝细胞凋亡指数（AI）。结果与CN组和SO组比较,BDL组大鼠血浆TBIL、ALT、AST、AKP、GGT水平和肝组织MDA含量明显升高（P〈0.05,P〈0.01）,SOD、CAT、GSH-Px活力或GSH含量显著降低（P〈0.01）,AI增加（P〈0.01）;褪黑素治疗可使血浆TBIL、ALT、AST、AKP、GGT和肝组织MDA含量显著降低,SOD、CAT、GSH-Px活力或GSH含量明显升高（P〈0.01）,AI减少（P〈0.01）。BDL组肝组织MDA含量与血浆TBIL、ALT、AKP、AST、GGT水平均呈显著正相关（P〈0.01）,GSH、SOD、CAT、GSH-Px与血浆TBIL、ALT、AKP、ALT、AST水平分别均呈显著负相关（P〈0.01）;BDL组肝组织MDA含量的变化与AI呈正相关（P〈0.01）,而GSH含量及SOD、CAT、GSH-Px活力分别与AI呈负相关（P〈0.01）。结论大鼠梗阻性黄疸时,肝组织自由基大量产生介导的氧化性损伤及其细胞凋亡,参与了肝功能损害的发生、发展。褪黑素对大鼠梗阻性黄疸肝功能损害有一定程度的保护作用,其机制可能与其拮抗肝组织过氧化和细胞凋亡有关。     

葛根素对肝硬化大鼠肝脏缺血再灌注损伤保护作用及其保护机制的研究

目的观察葛根素（Pue）对肝硬化大鼠肝脏缺血再灌注损伤是否具有保护作用，及其保护机制。方法首先建立大鼠肝硬化动物模型，在此模型基础上建立大鼠全肝缺血再灌注模型，比较用Pue预处理对缺血再灌注后，肝组织光镜下的形态学改变；血清中丙氨酸氨基转移酶（ALT）、天冬氮酸氨基转移酶（AST）和氧化亚氮（NO）、丙二醛（MDA）含量、超氧化物歧化酶（SOD）活性，及肝组织中NO、肿瘤坏死因子α（TNF-α）、MDA含量、SOD活性变化。结果Pue预处理可使大鼠血清NO含量、肝组织NO含量及SOD活性明显增高；而血清ALT、AST、MDA含量及肝组织TNF—α、MDA含量明显降低；肝组织形态损伤也有所减轻。结论葛根素对肝硬化大鼠肝缺血再灌注损伤有显著的保护作用，其主要机制是减少NO的降低、扩张血管、改善微循环；清除氧自由基、减轻脂质过氧化。     

梗阻性黄疸对巨噬细胞活性和细菌移位的影响

目的：探讨梗阻性黄疸对巨噬细胞活性和细菌移位的影响。方法：小鼠胆总管结扎后第7d，测定血清总胆红素、白蛋白、谷草转氨酶、肌酐及碱性磷酸酶水平，取肝、肾病检，肠系膜淋巴结行细菌培养，并检测腹腔巨噬细胞体外产生NO水平。结果：胆总管结扎可显著升高血清总胆红素、谷草转氨酶和碱性磷酸酶水平（P＜0．01），降低白蛋白水平（P＜0．05），且引起胆管扩张和肝、肾组织炎性细胞浸润。实验组53．3％肠系膜淋巴结培养出大肠杆菌。实验组与对照组NO水平无显著差异（P＞0．05）；加入内毒素（1μg/ml)后，实验组NO水平显著低于对照组（P＜0．05）。结论：小鼠实验性梗阻性黄疸发生时，除引起肝功能异常和肝肾病理损害外，还可引起腹腔巨噬细胞活性下降和细菌移位。     

一氧化氮、内皮素-1和肝"筛"在鼠淤胆性肝纤维化中的作用

目的：探讨一氧化氮（NO）和内皮素-1（ET-1）在淤胆性肝纤维化中的作用。方法：将48只Wistar大鼠随机分成：对照组、胆总管结扎组及胆总管结扎加乳果糖组。观察术后第3，7，14和21d血浆内毒素，NO和ET-1水平及肝脏结构和功能的变化。结果：胆总管结扎致胆汁淤积后，随着血浆内毒素水平升高，NO和ET-1水平相应上升，血浆AST，ALT也明显升高。肝纤维化程度随梗阻时间逐渐加重。电镜下见肝窦变窄，Disse间隙增宽，内有大量胶原纤维沉积，肝“筛“的数量和直径均明显减少。使用乳果糖能部分逆转肝脏功能和结构的病理改变。结论：NO和ET-1可能通过作用于肝“筛“而引起淤胆性肝纤维化。     

内皮素、一氧化氮与阻塞性黄疸肾功能障碍关系的实验研究

目的 研究内皮素(Endothelin ET)、一氧化氮(Nitric Oxide NO)与阻塞性黄疸(Obstructive Jaundice OJ)肾功能障碍的关系。方法 雄性SD大鼠胆总管结扎后随机分成5天、10天、15天三组，同时建立对应的假手术对照组。观察肾功能的变化，同时测定血和肾组织ET、NO水平及一氧化氮合酶(Nitric Oxide Synthetase NOS)活性，并用图像分析检测ET—1mRNA和NOS—mRNA表达的部位和量的变化。结果 随胆总管梗阻时间的延长，血和肾组织ET升高，NO下降，ET／NO比值与内生肌酐清除率(Creatinine clearance rate Ccr)、肾皮质血流(Renal cortex blood flow RCBF)呈负相关。肾组织ET—1mRNA和iNOS mRNA表达增加，血和肾组织NOS活性降低。结论 血和肾组织ET升高，NO下降，ET／NO比值升高是导致OJ时肾功能损伤的原因之一。     

一氧化氮对急性肝功能衰竭大鼠生存的影响

目的探讨一氧化氮(NO)前体及一氧化氮合酶(NOS)抑制剂对急性肝功能衰竭(ALF)大鼠生存的影响.方法切除大鼠90%肝脏制备ALF模型,选用NO前体或NOS抑制剂诱导或抑制机体产生NO,观察在ALF时NO对大鼠肝、肺、肾、肠等重要脏器功能及生存期的影响.结果应用NO前体,ALF大鼠丙氨酸转氨酶(ALT)显著下降,肝、肺、肾、肠等重要脏器组织病理损害明显减轻,大鼠24 h、72     

牛磺酸对大鼠小肠缺血再灌注后肝、肾损伤的保护作用

摘要：目的:研究牛磺酸对大鼠小肠I/R后肝、肾损伤的保护作用。方法:雄性Wistar大鼠随机分为3组：假手术对照组（S组）、生理盐水对照组（I/R组）和牛磺酸保护组（T组）。T组术前30min经鼠阴茎背静脉注射2%的牛磺酸200mg/kg。采用肠系膜上动脉根部阻断1h后复流行再灌注的方法制作肠I/R模型。除S组外，其余2组分别于再灌注1.5,3,6,12h抽血测定ALT,AST,BUN及Cr值，评定肝、肾功能。肝、肾切片行HE染色，比较组织病理学差异。用原位末端标记（TUNEL）法测定肝、肾细胞凋亡百分率，评定平均光密度值。结果:I/R组与S组相比，血清ALT,AST,BUN及Cr值均明显升高（P<0.05 ），3h最高，以后开始下降，12h仍高于S组；肝、肾病理损伤I/R组也相应严重，肝、肾细胞TUNEL阳性表达率、平均光密度值明显增加 （P<0.05）。T组与I/R组相比，前者血清ALT,AST,BUN及Cr水平明显减低 (P<0.05)，病理损伤也相应较轻；肝、肾细胞TUNEL阳性表达率、平均光密度值明显减少(P<0.05)。结论:牛磺酸对大鼠小肠I/R后肝、肾损伤具有明显的保护作用。     

褪黑素对大鼠梗阻性黄疸肾损害的保护作用

目的　探讨一氧化氮 (NO)在大鼠梗阻性黄疸肾功能损害发生中的作用 ,以及褪黑素 (melatonin ,Mel)的保护作用。方法　 6 4只雄性SD大鼠随机均分为 4组 :正常对照组 (CN组 )、假手术组 (SO组 )、胆总管结扎组(BLD组 )和褪黑素治疗组 (BDL +Mel组 )。应用胆总管结扎法建立梗阻性黄疸模型 ,分别于手术后第 4天和第 8天两个时间点检测 4组中血浆NO、TB、DB、ALT、AST、BUN、Cr水平以及肾组织中NO水平和iNOS活性 ;光镜下观察肾组织病理形态改变。结果　BDL组大鼠血浆NO、TB、DB、ALT、AST、BUN、Cr水平和肾组织NO水平及iNOS活性明显升高 (P<0 .0 1) ,褪黑素治疗可使血浆NO、ALT、AST、BUN及Cr水平和肾组织中NO水平及iNOS活性显著降低 ,与BDL组比较差异有显著性意义 (P<0 .0 1)。结论　梗阻性黄疸时 ,肾组织iNOS活性增强 ,NO大量产生参与了肾功能损害的发生、发展 ;褪黑素对大鼠梗阻性黄疸肾损害的保护作用至少部分是通过干扰NO通路实现的。     

氨基胍对梗阻性黄疸大鼠治疗作用的实验研究

目的 探讨诱导型一氧化氮合酶(iNOS)抑制剂氨基胍(AG)对梗阻性黄疸大鼠的治疗作用及作用机制.方法 雄性Wistar大鼠40只,随机分为正常对照组、假手术组、黄疸组、氨基胍治疗组4组,每组10只.通过测定治疗前后肝功、血胆红素、内毒素、乳酸、肝组织丙二醛水平,以及通过对肝脏、小肠的形态学分析来探讨氨基胍对梗阻性黄疽大鼠的治疗作用.结果 血浆内毒素和血清乳酸、肝组织丙二醛随着胆道梗阻时间的延长逐步升高,并伴随着肝脏小肠病理形态学的改变.氨基胍治疗组各项指标显著低于对照组,并能改善肝组织及小肠病理形态.结论 氨基胍(AG)可通过减轻脂质过氧化与内毒素血症发挥保护肝脏及小肠的作用,为治疗梗阻性黄疸患者提供了一种新的思路和方法.     

氨基胍对梗阻性黄疸大鼠治疗作用的实验研究

目的 探讨诱导型一氧化氮合酶(iNOS)抑制剂氨基胍(AG)对梗阻性黄疸大鼠的治疗作用及作用机制.方法 雄性Wistar大鼠40只,随机分为正常对照组、假手术组、黄疸组、氨基胍治疗组4组,每组10只.通过测定治疗前后肝功、血胆红素、内毒素、乳酸、肝组织丙二醛水平,以及通过对肝脏、小肠的形态学分析来探讨氨基胍对梗阻性黄疽大鼠的治疗作用.结果 血浆内毒素和血清乳酸、肝组织丙二醛随着胆道梗阻时间的延长逐步升高,并伴随着肝脏小肠病理形态学的改变.氨基胍治疗组各项指标显著低于对照组,并能改善肝组织及小肠病理形态.结论 氨基胍(AG)可通过减轻脂质过氧化与内毒素血症发挥保护肝脏及小肠的作用,为治疗梗阻性黄疸患者提供了一种新的思路和方法.

Abstract：

Objective To evaluate the therapeutic effect and mechanism of specific inducible nitric oxide synthase(iNOS)aminoguanidine(AG)in rats with obstructive jaundice.Methods Forty male Wistar rats were divided randomly into four groups: normal control group, sham operation group, obstructive jaundice group and aminoguanidine therapeutic group.Each group had 10 rats.We assayed levels of liver function,hemobilirubin, endotoxin,lactic acid and malondialdehyde before and after therapy, and we also analyzed pathology of the liver and small intestine.Then we could explore the therapeutic effect of AG in rats with obstructive jaundice.Results The levels of endotoxin,lactic acid and malondialdehyde in blood increased progressively along with the pathological changes of the liver and small intestine.Each of the AG group parameters was significantly lower, and the pathological changes of liver and small intestine were improved.Conclusion AG could protect liver and small intestine by attenuating lipid peroxidative and endotoxemia,and provide a new way to cure obstructive jaundice.     

The effect of aminoguanidine on blood and tissue lipid peroxidation in jaundiced rats with endotoxemia induced with LPS.

Obstructive jaundice (OJ) is a severe condition that leads to several complications. One of the important problems in OJ is the increased incidence of endotoxemia, which is the result of bacterial translocation (BT) and defective host immune response. Lipid peroxidation (LP) is an important problem in OJ and sepsis in which nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) activity are increased and antioxidative activity is decreased. Formation of peroxynitrite (ONOO(-)) anion leads to cellular damage and apoptosis. In this experimental study, we explore the effect of specific iNOS inhibitor aminoguanidine (AG) on blood and tissue (liver and renal) LP and iNOS levels in jaundiced rats with endotoxemia induced with lipopolysaccharide (LPS). Rats were randomized into six groups; group A, sham; group B, obstructive jaundice (OJ); group C, OJ + LPS; group D, OJ + AG; group E, OJ + LPS + AG; group F, OJ + AG + LPS. Serum malondialdehyde (MDA) and serum myeloperoxidase (MPO) activity and liver and renal tissue MDA, MPO, and Na(+)/K(+)-ATPase activity levels were detected in biochemical methods. Liver and renal tissue iNOS levels were examined immunohistopathologically. Serum and tissue MDA and MPO levels and tissue iNOS expression were increased significantly in groups B, C, and E, while tissue ATPase levels were decreased significantly in the same groups. In the group treated with AG (group D), serum and tissue MDA and MPO levels and tissue iNOS expression were decreased while tissue ATPase levels were increased significantly. In group F, if AG was administrated before LPS, we observed that serum and tissue MDA and MPO levels and tissue iNOS expression were decreased while tissue ATPase levels were increased significantly. Thus, our study showed that AG had a protective effect when it was administrated before LPS, but it failed to prevent tissue iNOS expression and LP if there was established endotoxemia in OJ.     

The Effect of Aminoguanidine on Blood and Tissue Lipid Peroxidation in Jaundiced Rats With Endotoxemia Induced With LPS

Obstructive jaundice (OJ) is a severe condition that leads to several complications. One of the important problems in OJ is the increased incidence of endotoxemia, which is the result of bacterial translocation (BT) and defective host immune response. Lipid peroxidation (LP) is an important problem in OJ and sepsis in which nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) activity are increased and antioxidative activity is decreased. Formation of peroxynitrite (ONOO^?) anion leads to cellular damage and apoptosis. In this experimental study, we explore the effect of specific iNOS inhibitor aminoguanidine (AG) on blood and tissue (liver and renal) LP and iNOS levels in jaundiced rats with endotoxemia induced with lipopolysaccharide (LPS). Rats were randomized into six groups; group A, sham; group B, obstructive jaundice (OJ); group C, OJ + LPS; group D, OJ + AG; group E, OJ + LPS + AG; group F, OJ + AG + LPS. Serum malondialdehyde (MDA) and serum myeloperoxidase (MPO) activity and liver and renal tissue MDA, MPO, and Na⁺/K⁺-ATPase activity levels were detected in biochemical methods. Liver and renal tissue iNOS levels were examined immunohistopathologically. Serum and tissue MDA and MPO levels and tissue iNOS expression were increased significantly in groups B, C, and E, while tissue ATPase levels were decreased significantly in the same groups. In the group treated with AG (group D), serum and tissue MDA and MPO levels and tissue iNOS expression were decreased while tissue ATPase levels were increased significantly. In group F, if AG was administrated before LPS, we observed that serum and tissue MDA and MPO levels and tissue iNOS expression were decreased while tissue ATPase levels were increased significantly. Thus, our study showed that AG had a protective effect when it was administrated before LPS, but it failed to prevent tissue iNOS expression and LP if there was established endotoxemia in OJ.     

Effect of Oral Glutamine Administration on Bacterial Tanslocation, Endotoxemia, Liver and Ileal Morphology, and Apoptosis in Rats with Obstructive Jaundice

Postoperative complications in patients with obstructive jaundice remain increased when associated with endotoxemia and the inflammatory response due to gut barrier failure. Administration of glutamine has been proposed to maintain the integrity of the gut mucosa and thus reduce bacterial translocation (BT), but the effects of this pretreatment on apoptosis and histologic morphology of various organs affected by BT in obstructive jaundice have not been studied. We therefore studied the effects of oral glutamine supplementation on endotoxemia, BT, liver and terminal ileal morphology, and apoptosis in an experimental model of obstructive jaundice. A total of 60 male Wistar rats were randomly divided into four groups of 15 each: I, controls; II, sham-operated; III, bile duct ligation (BDL); IV, BDL + glutamine (4.5 g/kg/day in drinking water). Ileal samples for histology, DNA and protein content, liver biopsies, mesenteric lymph nodes (MLNs) for culture, and portal and systemic blood samples for endotoxin measurements were obtained 10 days later. Compared to the controls, a significant increase in contaminated MLN and liver samples and increased endotoxemia were noted in group III (p < 0.01) but were significantly reduced in group IV (p < 0.05). Group IV also had a significantly higher number of mitoses per crypt (M/c) (p < 0.05), less apoptotic body counts (ABCs) (p < 0.05), and a higher DNA content than did group III (p < 0.05). Liver biopsies from group III displayed typical changes of large duct obstruction that significantly improved after glutamine treatment, with decreased ductular proliferation. We concluded that supplementation of oral glutamine in the presence of obstructive jaundice ameliorates BT, endotoxemia, and apoptosis and improves the ileal and liver histology.     

蛙皮素对梗阻性黄疸大鼠的肝脏保护性实验研究

目的探讨蛙皮素对梗阻性黄疸大鼠肝脏的保护作用。方法40只Wistar雄性大鼠随机分成4组：正常组、假手术组、阻黄组、阻黄＋蛙皮素治疗组。术后第10天，检测下腔静脉血ALT、BIL-T、LPS值，测定肝脏氧化应激SOD、MDA、GSH、GST水平，光镜观察肝脏组织结构，免疫组化表达肝脏MCP-1。结果蛙皮素降低ALT、LPS水平，减轻肝脏氧化应激，减少汇管区炎症细胞浸润，弱化MCP-1免疫组化阳性表达，对BIL-T无影响。讨论蛙皮素对梗阻性黄疸大鼠肝脏损伤有保护作用，这一结果为l临床治疗胆道梗阻肝脏损害提供一种新的方法。     

胆道梗阻早期大鼠MCP-1、TGF-β1的表达及意义

目的 探讨炎性趋化因子MCP-1及致纤维化因子TGF-β1在胆道梗阻早期大鼠中的表达及与肝脏损伤相应指标的关系.方法 50只Wistar雄性大鼠随机分为3组:正常组、假手术组和胆道梗阻组.术后10 d,各组大鼠检测血清ALT和BIL-T值,肝脏匀浆组织测得MDA含量,酶联免疫吸附试验反应血清TGF-β1指标,免疫组化表达肝脏MCP-1的浸润程度.结果 相比正常组及假手术组大鼠的各检测指标,早期胆道梗阻组大鼠肝脏MDA含量、MCP-1表达强度及血清ALT、BIL-T、TGF-β1水平均升高.胆道梗阻早期大鼠肝脏MCP-1表达与血清ALT及BIL-T升高有关,MCP-1高表达还与肝脏氧化应激指标MDA含量增加有关.血清TGF-β1水平升高只与血清ALT及BIL-T数值增加相关.而与MDA含量增加无关.结论 胆道梗阻早期大鼠肝脏MCP-1高表达及血清TGF-β1指标升高均与肝脏损伤及胆汁淤积有关,同时MCP-1的高表达还与肝脏氧化应激一致,二者对胆道梗阻早期肝脏损伤机制研究有重要意义.     

The effect of temporary hepatic artery or portal vein occlusion in obstructive jaundice.

Hepatic hemodynamics before vascular occlusion and the effect of transient hepatic artery or portal vein occlusion on the liver were investigated in normal dogs and dogs with experimentally induced obstructive jaundice by measurement of hepatic tissue blood flow (HTBF), index of hemoglobin concentration (IHb), oxygen saturation (ISO2), serum glutamic pyruvic transaminase (SGPT) concentration, and malonaldehyde (MDA) concentration in liver tissue. Livers with obstructive jaundice had increased blood flow and a lower hemoglobin concentration compared with normal livers at baseline before vascular occlusion. Percentage change of ISO2 from baseline was higher than percentage change of HTBF after reperfusion in both normal and obstructive jaundiced liver, although they were decreased to almost similar proportions during vascular occlusion. MDA concentration in obstructive jaundice after reperfusion following vascular occlusion was higher than in normal liver. Furthermore, MDA concentration after reperfusion following hepatic artery occlusion was increased compared with after reperfusion following portal venous occlusion in obstructive jaundice. There was no evidence of massive liver necrosis which was newly developed by transient vascular occlusion. These results represent the pathological condition in the liver before transient vascular occlusion and after reperfusion in obstructive jaundice.     

Effect of different enteral nutrients on bacterial translocation in experimental obstructive jaundice

Obstructive jaundice leads to bacterial translocation (BT) by disruption of the gut barrier, intestinal microecology, and impaired host immune defence. The objective of the present study is to investigate the effects of different enteral nutrients on BT that is induced by obstructive jaundice in rats. Eighty male Wistar-Albino rats were randomly assigned into 4 groups. Group 1: 20 rats underwent laparotomy, common bile duct (CBD) was not actually ligated and transected, but sham ligation of CBD was performed. Groups 2-4: 60 rats underwent laparotomy, CBD ligation and transection. Group 1 and 2 rats were given rat chow, group 3 rats were fed a glutamine and arginine supplemented enteral diet, and group 4 rats were fed an arginine, m-RNA and omega-3 supplemented enteral diet, an immunonutrient. Rats in groups 3 and 4 had significantly less BT to mesenteric lymph nodes compared to rats in group 2 (p = 0.001). These findings suggest that oral administration of an arginine and glutamine supplemented diet and immunonutrition reduce BT in rats with obstructive jaundice.     

梗阻性黄疸大鼠可溶性Fas与肝肾功能改变的关系

目的:探讨可溶性Fas(sFas)与梗阻性黄疸大鼠肝肾功能损害的关系.方法: 将雄性SD大鼠36只随机分为对照组(A组)、胆总管结扎节第7天组(B组)和第21天组(C组 ),每组12只.分别检测各组血清胆红素、ALT、白蛋白、肌酐、尿素氮和sFas.光镜观察肝肾组织的病理改变. 结果B组胆红素、ALT和sFas较A组显著升高(P<0.01 );C组胆红素、ALT、肌酐、尿素氮和sFas较A组显著升高(P<0.01).B组和C组部分肝细胞和肾小管上皮细胞肿胀和坏死,C组较严重. 结论sFas与梗阻性黄疸大鼠肝肾功能损害相关,可能通过细胞凋亡起作用 .