热应激预处理对梗阻性黄疸大鼠T细胞亚群的影响

目的:研究热应激预处理对梗阻性黄疸大鼠细胞免疫功能的影响.方法:将30只Wistar大鼠随机均分为3组:假手术组(S组)、胆总管结扎组(B组)、热应激预处理 胆总管结扎组(P组).术后1wk处死大鼠穿刺心脏取血,用流式细胞仪检测各份血液标本的T淋巴细胞(CD4 、CD8 )分类及胆红素含量.结果:胆总管结扎后1wk,大鼠血胆红素明显升高,CD4 减少,CD4 /CD8 下降;热应激预处理组的CD4 、CD4 /CD8 下降不明显,但与胆总管结扎组比较有显著差异(52.60±3.27vs43.52±2.23,2.37vs1.96;P<0.01).鼠T细胞亚响,目前尚关报道.结论:热应激预处理可改善梗阻性黄疸大鼠的细胞免疫功能.     

梗阻性黄疸对肠黏膜屏障的影响

肠黏膜屏障包括机械屏障、免疫屏障、生物屏障和化学屏障,四者共同维持肠黏膜的正常防御功能。梗阻性黄疸患者引起肠黏膜屏障损伤,导致细菌移位及内毒素血症,后者又加重屏障功能障碍。本文主要就梗阻性黄疸对肠黏膜屏障损伤的机制作一综述。     

肺癌转移致梗阻性黄疸3例

梗阻性黄疸是肝胆外科常见的临床症状,其主要原因是胆道及胆总管结石和胆道、胰头部及十二指肠乳头部肿瘤.肺癌转移至胰头、壶腹周围等引起梗阻性黄疸临床少见.常规而认真的检查如胸部X线片及CT扫描是发现肺部原发肿瘤的主要方法,可减少漏诊,应引起临床上的重视.     

姜黄素对梗阻性黄疸大鼠肠黏膜屏障的保护作用

目的:探讨姜黄素对梗阻性黄疸(obstructive jaundice,OJ)大鼠小肠黏膜屏障的保护作用.方法:将♂SD大鼠随机分为3组:假手术对照(sham operation,SO)组、OJ组、姜黄素治疗(curcumin treatment,Cur)组.光镜下观察小肠组织形态学改变,测量肠绒毛高度和黏膜厚度,采用鲎试剂法检测血浆内毒素水平,采用放射免疫法检测血清肿瘤坏死因子-α(tumor necrosis factor-α,T N F-α)、白介素-6(interleukin-6,I L-6)水平,应用分光光度法测定肠组织二胺氧化酶(diamine oxidase,DAO)活性,采用免疫组织化学方法检测小肠组织中核因子-κB(nuclear factor kappa B,NF-κB)和细胞黏附分子-1(intercellular adhesion molecule-1,ICAM-1)的表达.结果:OJ组肠黏膜绒毛排列紊乱,绒毛稀疏、断裂,肠黏膜萎缩,绒毛水肿,部分上皮细胞坏死脱落,并可见炎性细胞浸润;Cur组肠黏膜病变较OJ组明显减轻,肠黏膜绒毛排列整齐,肠黏膜增厚,绒毛轻度水肿,未见明显上皮细胞脱落,炎性细胞浸润减少;与S O组比较,O J组内毒素、T N F-α、I L-6明显增高(P0.01),DAO活性、肠绒毛高度及黏膜厚度明显降低(P0.01);Cur组较OJ组内毒素、TNF-α、IL-6明显下降(P0.05或0.01),D A O活性、肠绒毛高度及黏膜厚度明显升高(P0.05).OJ组回肠黏膜NF-κB及ICAM-1表达明显高于SO组(P0.01);Cur组NF-κB及ICAM-1表达明显低于OJ组(P0.05或0.01).结论:姜黄素通过抑制NF-κB、TNF-α、IL-6和ICAM-1等炎症介质,对小肠黏膜屏障具有保护作用.     

梗阻性黄疸对大鼠周围神经结构的影响

将30只Wistar大鼠随机分为对照组、假手术组、梗阻性黄疸（OJ）组,每组10只。OJ组大鼠于近肝门处游离并结扎胆总管,假手术组仅做游离但不结扎胆总管。对照组、假手术组大鼠术后体质量上升,OJ组体质量显著降低,与术前相比P均〈0.05。OJ组大鼠术后血清直接胆红素、胆汁酸、内毒素水平显著高于正常对照组和假手术组,P均〈0.01。OJ组神经损伤较重。认为梗阻性黄疸大鼠存在周围神经变性,与内毒素移位和高胆红素血症有关。     

ERCP在梗阻性黄疸病因鉴别诊断中的应用

目的:探讨逆行胰胆管造影术(endoscopic retrograde cholangiopancreatogahpy,ERCP)在梗阻性黄疸的病因鉴别诊断中的应用价值.方法:行ERCP检查并经术后或病理检查确诊的梗阻性黄疸患者49例,其中40例行ERCP、B超、CT检查,比较分析三者的诊断符合率.结果:40例患者同时行ERCP、B超、CT检查,三种影像学诊断符合率分别为77.7%、35.72%、64.77%,其中ERCP对梗阻性黄疸病因的诊断率明显高于B超及CT检查(P<0.05).结论:ERCP在梗阻性黄疸的病因鉴别诊断中具有较高的诊断价值.且优于B超和CT检查.     

门静脉动脉化重建肝血流对梗阻性黄疸大鼠肝脏血液动力学的影响

目的:探讨用门静脉动脉化重建肝血流对肝脏血流动力学的影响.方法:大鼠40只,随机分为4组,每组各10只,第l组:对照组;第2组:单纯梗阻性黄疸5 d组;第3组:梗阻性黄疸术后5 d,行胆总管再通,并游离门腔静脉、结扎肝总动脉:第4组:梗阻性黄疸术后5 d,行胆总管再通,并行门静脉动脉化.对大鼠的一般情况、肝脏的结构和功能的改变、肝脏血流量和门静脉压及肝脏微血管的影响进行为期1mo的观察.结果:大鼠在胆总管结扎5 d后,胆红素(T-BIL、D-BIL)、转氨酶(ALT、AST)和碱性磷酸酶(ALP)显著增高(141.7±10.6vs6.7±2.1.68.16±7.6vs3.25±1.7.132±22vs53±8.160±38vs73±16,285±60vs148±4l,均P＜0.01).胆总管结扎5 d后的大鼠行胆管再通+门静脉动脉化手术后1 mo,肝脏血流量和门静脉压与正常组比较无显著差异.血管铸型标本显示肝窦略变粗,较正常更为充盈,虽有一定的变形,但仍呈放射状分布在中央静脉的周围.结论:门静脉动脉化后1 mo对肝脏的血流动力学和肝脏的微血管不会造成明显的不良影响.肝脏功能和结构可顺利恢复.     

梗阻性黄疸大鼠NF-κB的变化及其对免疫应答的影响

目的:探讨梗阻性黄疸(obstructive jaundice,OJ)时NF-KB的变化及其对免疫应答的影响.方法:60只Wistar♂大鼠随机分成3组:假手术组(SHAM组)、梗阻性黄疸组(CBDL组)和梗阻性黄疸+NF-kB抑制剂脯氨酸二硫化氨基甲酸酯(PDTC)组(PDTC组).每组术后7、14 d分批(n=10)检测光镜下肝脏病理组织学,血清总胆红素(TB),谷丙转氨酶(ALT),内毒素(LPS)水平,肝组织促炎因子IL-1β、IL-6,抑炎因子IL-10以及NF-kB蛋白表达.结果:CBDL组7、14 d大鼠均出现肝组织病理损伤,CBDL组较SHAM组血清TB、ALT、LPS增高(7 d:140.14±10.17 vs 7.309±1.04,134.479±10.20 vs 35.79±3.76.189.33±11.05 vs 2.816±0.58;14 d:194.608±12.73 vs 36.142±3.51.217.797±12.37 vs 7.321±1.03.292.816±14.53vs 2.664±0.53,均P＜0.01),肝组织IL-1β,IL-6,IL-10和NF-kB表达增强(均P＜0.01),且14 d较7 d变化更为显著.PDTC组大鼠血清TB、ALT和肝组织IL-1β、IL-6、NF-kB表达在7 d时相点时比CBDL组显著下降(P＜0.01),而到14 d时相点时比较CBDL组无明显变化;LPS和IL-10表达与CBDL组各时相点相比无明显差异.结论:梗阻性黄疸大鼠早期(7 d)通过PDTC抑制NF-kB活化表达,可下调促炎因子的表达,减轻肝损.后期(14 d)作用不明显,其机制可能是通过LPS、IL-10等其他途径所致.     

急慢性大鼠梗阻性黄疸模型的建立

目的:探讨急慢性SD大鼠梗阻性黄疸模型的建立,评价其模拟临床梗阻性黄疸的价值,提供一种新型的慢性梗阻性黄疸模型.方法:SD大鼠随机分成3组,每组每时段6只:急性梗阻性黄疸模型组(A组),慢性梗阻性黄疸模型组(B组),对照组(C组).造模后于第1、2、3、4、5周分别抽取大鼠静脉血检查肝功能,显微镜下刻度目镜检测大鼠胆总管直径,光学显微镜观察肝组织的病理改变,其中第4周行胆总管十二指肠吻合再通.结果:A组造模术后4wk内黄疸进行性加重(TB:749.38μmol/L±38.99μmol/Lvs84.86μmol/L±49.09μmol/L,P<0.05),胆总管直径扩张明显(1.50cm±0.30cmvs0.35cm±0.15cm,P<0.05),肝细胞变性、坏死明显,伴有增生.第4周行胆总管与十二指肠端侧吻合后黄疸消退明显(TB:153.93μmol/L±57.36μmol/Lvs749.38μmol/L±38.99μmol/L).B组造模术后黄疸呈现波动性,胆总管直径扩张(0.20cm±0.15cmvs0.30cm±0.10cm,P<0.05),肝细胞以变性为主,并有纤维组织增生.第4周行胆总管与十二指肠端...     

梗阻性黄疸肠黏膜屏障损伤病理生理机制的研究进展

肠黏膜屏障具有机械屏障、化学屏障、生物屏障、免疫屏障等功能,是防止肠道内的有害物质和病原体进入机体内环境,维持内环境稳定的一道重要屏障.梗阻性黄疸(obstructive jaundice,OJ)患者病死率和并发症发生率居高不下,主要原因是败血症和肾功能衰竭.临床与基础研究证实OJ存在肠黏膜屏障损伤,其主要病理生理机制是肠黏膜通透性增加、肠黏膜上皮氧化应激损伤及肠源性内毒素血症,具体机制尚未明确.本文对OJ引起的肠黏膜屏障损伤的病理生理机制作一综述.     

Pathophysiological consequences of obstructive jaundice and perioperative management

Background: Obstructive jaundice is a common problem in daily clinical practice. Understanding completely the pathophysiological changes in obstructive jaundice remains a challenge for planning current and future management.Data sources: A Pub Med was searched for relevant articles published up to August 2016. The effect of obstructive jaundice on proinflammatory cytokines, coagulation status, hemodynamics and organ functions were evaluated.Results: The effects of obstructive jaundice included biliary tree, the hepatic cell and liver function as well as systemic complications. The lack of bile in the gut, the disruption of the intestinal mucosal barrier,the increased absorption of endotoxin and the subsequent endotoxemia cause proinflammatory cytokine production(TNF-α, IL-6). Bilirubin induces systemic inflammatory response syndrome which may lead to multiple organ dysfunction syndrome. The principal clinical manifestations include hemodynamic instability and acute renal failure, cardiovascular suppression, immune compromise, coagulation disorders,nutritional impairment, and wound healing defect. The proper management includes full replacement of water and electrolyte deficiency, prophylactic antibiotics, lactulose, vitamin K and fresh frozen plasma,albumin and dopamine. The preoperative biliary drainage has not been indicated in overall, but only in a few selected cases.Conclusion: The perioperative management is an essential measure in improving the outcome after the appropriate surgical operation in jaundiced patients especially those with malignancy.     

Hyperbaric oxygen prevents bacterial translocation in rats with obstructive jaundice

This study was designed to demonstrate bacterial translocation following bile duct ligation and investigate preventive effects of hyperbaric oxygen on obstructive jaundice-related bacterial translocation in an animal model. Hyperbaric oxygen treatment significantly reduced the endogenous colony counts in distal ileum of normal rats both in the short (two days) and long (seven days) term. Endogenous bacteria in distal ileum significantly increased in bile duct ligated rats in the short and long term, and presence of bacterial translocation was proven by bacterial growth in mesenteric lymph nodes, liver, spleen, and blood. Short- and long-term hyperbaric oxygen treatments significantly reduced the intestinal colony counts and prevented the bacterial translocation almost completely in rats with bile duct ligation. It is concluded that obstructive jaundice causes bacterial overgrowth and translocation, and hyperbaric oxygen treatment can prevent both bacterial overgrowth and translocation effectively.     

Effects of glutamine and curcumin on bacterial translocation in jaundiced rats

AIM: To investigate the effect of curcumin on bacterial translocation and oxidative damage in an obstructive jaundice model and compare the results to glutamine, an agent known to be effective and clinically used. METHODS: Twenty-four female Wistar-Albino rats, weighing 200-250 g, were randomly divided into three groups (8 in each group). After ligation of the common bile duct in all animals, GroupⅠ received oral normal saline, Group Ⅱ received oral glutamine and Group Ⅲ received oral curcumin for seven day...     

rhGH对梗阻性黄疸患者术后免疫功能的影响

目的: 探讨重组人生长激素(rhGH)对梗阻性黄疸患者术后免疫功能的影响及临床意义.方法: 采用前瞻、随机、对照方法,对入选36例患者分为对照组(A组,n = 18)、rhGH组(B组,n = 18),B组加用rhGH,检测2组治疗前和治疗后1、8 d细胞免疫指标(CD3+、CD4+、CD4+/CD8+)、体液免疫指标(IgM、IgA、IgG)和免疫调节因子(IL-2、IL-6、TNF-α)的动态水平,并观察2组患者并发症和病死率的变化.结果: B组治疗后8 d与A组比较,CD3+、CD4+、CD4+/CD8+指标升高水平明显(42.32%±4.19% vs 31.51%±4.42%;26.36%±4.25%vs 19.29%±4.27%;1.22±0.20 vs 0.95±0.12,均P<0.05);IgA、IgG和IgM浓度明显升高(2.42±0.11 g/L vs 1.41±013 g/L;6.88±0.18g/L vs 4.89±0.15 g/L;1.84±0.18 g/L vs 1.28±0.24 g/L,均P<0.05);IL-6和TNF-α下降明显(0.42±0.11 mg/L vs 0.86±0.10 mg/L;11.04±1.52 pmol/L vs 18.24±1.22 pmol/L,均P<0.05),IL-2浓度显著升高(1.92±0.15 mg/L vs 1.14±0.12 mg/L,P<0.05);B组并发症发生率和病死率明显低于A组(22.22% vs 44.44%,0.00% vs5.56%,均P<0.05).结论: rhGH对梗阻性黄疸患者术后免疫功能具有直接的调理作用,能明显改善患者的免疫状态,有利于患者康复.     

Mechanism of pancreatic hypersecretion in dogs with obstructive jaundice

Summary Pancreatic exocrine function in experimental obstructive jaundice was examined using dogs. Outputs of pancreatic juice, bicarbonate and amylase were greater in dogs with obstructive jaundice than in control dogs. To further examine the hypersecretory mechanism in obstructive jaundice, we examined pancreatic exocrine secretion stimulated by secretin and pancreozymin in both the isolated perfused pancreas and pancreatic dispersed cell culture. The perfused pancreas stimulated with secretin and pancreozymin in dogs with obstructive jaundice showed higher secretion of volume, bicarbonate and amylase than in control dogs. Dispersed pancreatic cells of jaundiced dogs stimulated by secretin and pancreozymin released more bicarbonate and amylase into the media than dispersed cells of control dogs. These data suggest pancreatic hypersecretion in obstructive jaundice is not due to excessive serum levels of secretin and pancreozymin or impaired metabolism of these hormones.     

Diagnosis and initial management of cholangiocarcinoma with obstructive jaundice

Cholangiocarcinoma is the second most common primary hepatic cancer. Despite advances in diagnostic techniques during the past decade, cholangiocarcinoma is usually encountered at an advanced stage. In this review, we describe the classification, diagnosis, and initial management of cholangiocarcinoma with obstructive jaundice.     

阻塞性黄疸与消化性溃疡

目的证实消化性溃疡与阻塞性黄疸的相关性。方法经内镜证实的溃疡患者289例，从无溃疡患者中随机挑选290例设为对照组，进行去除混杂因素的非条件的logistic回归分析。比较消化性溃疡各病种之间与阻塞性黄疸发生率的差异，消化性溃疡中的高位梗阻与低位梗阻发生率的差异，溃疡组与无溃疡组的肝功能各项指标的对比，黄疸的发生时间与消化性溃疡发生的关系，以及胃溃疡与十二指肠溃疡发生率的差异。结果溃疡组的阻塞性黄疸发病率及黄疸指数明显高于对照组（P〈0．01），低位梗阻与高位梗阻对比，低位梗阻患者的消化性溃疡发生率高（P〈0．01），十二指肠与胃溃疡发生率两组有显著差别，各病种间的溃疡发生率有明显差别，溃疡的发生率与黄疸持续的时间相关。结论本研究进一步证实了消化性溃疡与阻塞性黄疸有明显的相关性，梗阻性黄疸导致高胃酸在十二指肠溃疡形成中的重要作用。     

Glucagon-like peptide-2 protects impaired intestinal mucosal barriers in obstructive jaundice rats

AIM: To observe the protective effect of glucagon-like peptide-2(GLP-2) on the intestinal barrier of rats with obstructive jaundice and determine the possible mechanisms of action involved in the protective effect.METHODS: Thirty-six Sprague-Dawley rats were randomly divided into a sham operation group, an obstructive jaundice group, and a GLP-2 group; each group consisted of 12 rats. The GLP-2 group was treated with GLP-2 after the day of surgery, whereas the other two groups were treated with the same concentration of normal saline. Alanine aminotransferase(ALT), total bilirubin, and endotoxin levels were recorded at 1, 3, 7, 10 and 14 d. Furthermore, on the 14 th day, body weight, the wet weight of the small intestine, pathological changes of the small intestine and the immunoglobulin A(Ig A) expressed by plasma cells located in the small intestinal lamina propria were recorded for each group.RESULTS: In the rat model, jaundice was obvious, and the rats’ activity decreased 4-6 d post bile duct ligation. Compared with the sham operation group, the obstructive jaundice group displayed increased yellow staining of abdominal visceral serosa, decreased small intestine wet weight, thinning of the intestinal muscle layer and villi, villous atrophy, uneven height, fusion, partial villous epithelial cell shedding, substantial inflammatory cell infiltration and significantly reduced Ig A expression. However, no significant gross changes were noted between the GLP-2 and sham groups. With time, the levels of ALT, endotoxin and bilirubin in the GLP-2 group were significantly increased compared with the sham group(P < 0.01). The increasing levels of the aforementioned markers were more significant in the obstructive jaundice group than in the GLP-2 group(P < 0.01).CONCLUSION: GLP-2 reduces intestinal mucosal injuries in obstructive jaundice rats, which might be attributed to increased intestinal Ig A and reduced bilirubin and endotoxin.     

急性胆道梗阻肠黏膜屏障破坏与氯离子通道-2的关系

目的:探讨急性胆道梗阻肠黏膜屏障破坏与肠上皮细胞氯离子通道-2(chloride channel-2,CLC-2)的关系.方法:建立急性胆道梗阻(阻塞性黄疸)大鼠动物模型,术后7d连续注射Lubiprostone(Lu组)、类高血糖素多肽-2(GLP-2组)、两者共同使用(Lu+GLP组),以假手术组(Sham组)和阻...