阻塞性黄疸鼠肠粘膜免疫功能的变化

ＳＤ大分为为阻塞性黄疸组和对照组，胆总管结扎制造阻塞性黄疸模型，以胆汁外引流组为对照，制模后２周，检测小肠液分泌型ＩｇＡ浓度、肠粘膜内淋巴细胞体外刺激转化能力、粘膜固有层淋巴细胞亚群。     

烧伤后肠粘膜免疫组织细胞增殖分化的研究

目的对烧伤后肠粘膜免疫组织潘氏结内淋巴细胞(PPL)膜IgA转型以及肠固有层的淋巴细胞(LPL)体外增殖情况进行观察,为提高粘膜免疫屏障水平、预防肠源性感染的发生提供依据.方法无特殊病原菌(SPF)小鼠,随机分为对照组(10只),烧伤组(10只).烧伤组致以20%TBSAⅢ度烧伤,于伤后3d与对照组同时活杀,用免疫组化染色观察肠固有层中IgA型浆细胞;PP中淋巴细胞表面IgA流式细胞计数;烧伤后LP淋巴细胞体外增殖检测;肠组织中IL-6 ELISA测定.结果PP中淋巴细胞表面IgA阳性率烧伤后3d低于正常对照组;烧伤后LP中IgA浆细胞数明显少于伤前的水平;烧伤后动物的LP中淋巴细胞体外增殖明显下降;烧伤后3d肠组织中IL-6水平与正常对照组无显著差别.结论烧伤后抑制肠粘膜免疫组织淋巴细胞自身的增殖、分化,导致粘膜免疫屏障水平降低.     

糖皮质激素对细菌易位的影响

分泌型 IgA(SIgA)是粘膜免疫系统的主要组成部分,具有防止细菌、病毒附着粘膜上皮细胞的功能。全肠外营养时由于胆道 SIgA 减少及肠道粘膜固有层 IgA 同型浆细胞的排空,从而使细菌向肠系膜淋巴     

肠饲保存肠粘膜免疫力不管体内MAdCAM-1阻断淋巴细胞回归

淋巴细胞对小肠粘膜下集合淋巴结的抗原敏感 ,移走经肠系膜淋巴结而回归至肠固有层 ,凡种粘附分子 ,包括粘膜地址素 (addressin)细胞分子 1(MAd-CAM- 1)、L 选择素、α4 β7整合素、淋巴细胞功能相关抗原 - 1(LFA- 1)和细胞间粘附分子 - 1(ICAM- 1)等 ,调控粘膜免疫系统中淋巴细胞的运输 ,其中 MAd CAM-1是最关键分子之一 ,位于内皮细胞表面。设想缺乏肠饲的刺激可减少在肠相关淋巴组织 (GALT)和其他粘膜区的 MAd CAM- 1表达 ,导致淋巴细胞数减少和粘膜免疫功能的损害。作者观察不同营养途径对 MAd-CAM- 1表达的影响及 MAd C…     

阻塞性黄疸对肠道细菌及小肠粘膜组织的影响

为探讨阻塞性黄疸（简称阻黄）对肠道细菌及粘膜组织的影响，通过建立阻黄动物模型，观察阻黄大鼠肠道细菌移位以及小肠粘膜组织学变化。结果发现：阻黄组（ＢＤＬ）术后３周厌氧性细菌移位的阳性率（４３．７５％）显著高于假性手术组（ＳＬ）（０％），Ｐ＜０．０５；组织学检查显示ＢＤＬ组肠粘膜发生了实质性损害。提示：阻黄时肠道内胆盐缺乏导致肠道常驻菌过度繁殖，肠道粘膜屏障的损害以及机体免疫功能抑制可能是促进肠道细菌移位，导致阻黄时感染易感性增高的主要原因     

肠外营养对胃肠免疫的影响(肠道刺激的重要性)

粘膜分泌的IgA(S-IgA)是粘膜防御系统的重要组成。泪液,唾液,乳汁,胆汁和肠液均发现有S-IgA。大鼠S-IgA由肠壁固有层中浆细胞产生。肠道中存在的S-IgA90%来自胆汁。因长时间完全胃肠外营养(TPN)应用及与之有关的感染并发症增加,提出了下述问题,即这种治疗方式是否损害局部粘膜免疫力。本研究为测定营养给予的途径是否影响大鼠胆汁中S-IgA水平。作者把25只重100～150g雌性Fisher大鼠随机分三组。组Ⅰ鼠(N=9)给肠外营养。组Ⅱ鼠(N=8)经胃造瘘饲以与标准静脉营养液等热卡,等氮量食物。组Ⅲ鼠(N=6)经口随意进鼠食和水。每隔4天收集每个大鼠胆汁到第16天为止。第16天处死     

重组人生长激素对大鼠肠缺血再灌注后肠壁组织T淋巴细胞亚群和浆细胞的影响

目的　探讨肠道屏障功能损害时应用重组人生长激素(rhGH )对肠道免疫屏障中肠黏膜及固有层内T淋巴细胞亚群和浆细胞的影响。方法　将60只Wistar大鼠雌雄各半随机分为实验组和对照组,按实验天数(2、4、6d)又各分为3组,每组10只,以肠缺血再灌注模型造成肠道屏障功能损害的病理现象,实验组给与rhGH (每日1.3 3U/kg体重) ,观察回肠末端黏膜固有层内CD8+、CD4+、CD3 +T淋巴细胞数及IgA浆细胞的数量变化。结果　(1)实验组CD8+、CD4+、CD3 +T及IgA浆细胞第6天与第2、4天比较数量显著增多,差异有统计学意义(P <0 .0 5 )。(2 )实验组与对照组第6天,CD8+、CD4+T及IgA浆细胞的数量实验组均高于对照组,差异有统计学意义(P <0 .0 5 )。(3 )CD4+/CD8+比值第2天两组差异有统计学意义(P <0 .0 5 )。结论　肠道屏障功能损害时应用重组人生长激素能够调节肠黏膜的免疫屏障,其作用时间在第6天可能最明显     

鼠肝大部切除术后肠粘膜细胞免疫功能的变化及其与肠道细菌移位的关系

目的　探讨鼠肝大部切除术后空、回肠粘膜固有层细胞免疫功能的变化及其与肠道细菌移位的关系。方法　将 48只SD大鼠随机分为实验组和假手术组 ,每组 2 4只。实验组切除 70 %肝脏 ,假手术组除不切除肝脏外 ,其余手术步骤同实验组。分别于术后 6、12、2 4和 72h取两组大鼠 (n =6)空、回肠粘膜冰冻切片 ,而后行免疫组化染色 ,观察不同时相肠粘膜固有层CD3+ 、CD4+ 、CD8+ T淋巴细胞的数量及肝脏功能的变化。结果　实验组术后 2 4h和 72h ,其肠粘膜固有层CD3+ 、CD4+ 和CD8+ T淋巴细胞的数量较假手术组明显下降 (P<0 .0 5) ,而两组大鼠术后不同时相的ALT及AST变化 ,实验组明显高于假手术组 (P<0 .0 5)。结论　鼠肝大部切除 ( 70 % )术后 2 4h ,肠粘膜固有层CD3+ 、CD4+ 和CD8+ T淋巴细胞数量明显降低。这种细胞免疫功能降低所导致的肠粘膜屏障功能受损 ,可能是造成肠道细菌移位的原因之一     

重组人生长激素对大鼠肠道缺血再灌注后肠壁组织T淋巴细胞亚群和浆细胞凋亡的影响

目的探讨肠道屏障功能损害时应用重组人生长激素（rhGH）对肠道免疫屏障中肠黏膜及固有层内T淋巴细胞亚群和浆细胞凋亡的影响。方法将60只Wistar大鼠雌雄各半随机分为实验组和对照组，按实验天数又各分为3组，每组10只，以肠缺血再灌注模型造成肠道屏障功能损害的病理现象，实验组给予rhGH每日（1．33U／kg体重），采用免疫组织化学双染法观察回肠末端黏膜固有层内CD8^＋、CD4^＋、CD3^＋T淋巴细胞数及IgA浆细胞的凋亡数量变化。结果（1）对照组CD3^＋T淋巴细胞及IgA浆细胞的凋亡数量第6天明显高于第2、4天。差异有统计学意义（P〈0．01）。（2）实验组CD8^＋、CD4^＋T淋巴细胞的凋亡数量第6天明显低于第4天，差异有统计学意义（P〈0．01）。（3）实验组与对照组相比第2、4、6天IgA浆细胞的凋亡数量均明显减少。差异有统计学意义（P〈0．01）。实验组与对照组相比大鼠第2天CD8^＋、CD4^＋、CD3^＋T淋巴细胞的凋亡数量均减少，差异有统计学意义（P〈0．05，P〈0．01）。结论肠道屏障功能损害时应用重组人生长激素能够减少肠道免疫细胞的凋亡数量，对IgA浆细胞作用最明显。可能的作用时间在第6天。     

急性坏死型胰腺炎大鼠肠粘膜CD44 mRNA的表达及生长激素的作用

目的 观察急性坏死型胰腺炎（ANP）大鼠肠粘膜CD44 mRNA表达、并探讨其与肠粘膜T淋巴细胞亚群和病理形态学变化的关系及生长激素（GH）的作用。方法 SD大鼠54只，随机分为3组：假手术组（SO）；ANP组；ANP＋GH组（0．75U／kg体重）。大鼠胰胆管内逆行推注5％牛磺胆酸钠溶液（1ml/kg体重）制备ANP模型。术后6、12、24h分批处死。逆转录聚合酶链反应研究CD44 mRNA的表达。免疫组织化学观察肠粘膜T淋巴细胞亚群。结果 ANP组各时点CD44 mRNA表达较SO组显著降低（P＜0．05）。GH上调CD44 mRNA的表达。ANP组术后6、12、24h肠粘膜CD3、CD4、CD8细胞数较SO组显著减少（P＜0．05），而GH治疗组肠粘膜CD3、CD4、CD8细胞数与SO组差异无差异性（P＞0．05）。ANP组肠上皮破损明显，GH治疗组肠粘膜结构基本完整。结论 ANP大鼠肠粘膜CD44 mRNA表达降低，而GH维持肠粘膜上皮结构完整及粘膜免疫功能的作用可能与上调CD44 mRNA表达有关。     

Internal biliary drainage improves decreased number of gut mucosal T lymphocytes and MAdCAM-1 expression in jaundiced rats

BACKGROUND: Although the effect of preoperative biliary drainage in patients with obstructive jaundice is controversial, bacterial or endotoxin translocation is one of the main postoperative problem in jaundiced patients. Failure in gut barrier functions causes bacterial translocation; homing and distribution of T lymphocytes in the intestinal lamina propria are important for gut mucosal immune defense. This study was performed to examine whether bile regulates the numbers of T lymphocyte subsets or the expression of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) in experimental jaundice in rats with and without external and internal biliary drainage. METHODS: Four groups of Wistar rats were used: those that received a sham operation (SHAM), common bile duct ligation (CBDL), CBDL followed by external drainage (ED), and CBDL followed by internal drainage (ID). Numbers of CD4(+) and CD8(+) T lymphocytes and MAdCAM-1-positive cells in the lamina propria were counted immunohistochemically in the specimens of jejunum and ileum of each group. Bacterial translocation was examined by culturing from the mesenteric lymph node complex isolated from rats in each group. RESULTS: A significant decrease in numbers of CD4(+) and CD8(+) T lymphocytes and MAdCAM-1-positive cells in the lamina propria was seen in obstructive jaundice, although numbers of peripheral blood lymphocytes increased in comparison with the sham-operated control. The numbers of CD4(+) and CD8(+) T lymphocytes and MAdCAM-1 expression in the lamina propria did not recover to a normal level after external drainage, but did so after internal drainage. Frequencies of bacterial translocation were high in the CBDL and ED group. In contrast, bacterial translocation was not present in any animals in the SHAM group and was at a low percentage in the ID group. CONCLUSIONS: Changes in the number of T lymphocytes and MAdCAM-1 expression are associated with the presence of bile in the gastrointestinal tract and are inversely correlated with the frequency of bacterial translocation induced by CBD ligation. MAdCAM-1 expression maintained by the presence of bile may regulate T-lymphocyte homing to the lamina propria in obstructive jaundice.     

An improved rat model of obstructive jaundice and its reversal by internal and external drainage.

BACKGROUND: A simple and reproducible rat model that allows studies of the reversal of obstructive jaundice (OJ) by internal (ID) and external (ED) drainage is not available at present. METHODS: OJ was induced in rats by double ligation and division of the common bile duct. To minimize tissue handling and dissection the duodenum was extracted with a ophthalmic muscle hook and the common bile duct isolated using very fine forceps. One week after bile duct ligation, ID was accomplished by implanting a length of infant feeding tube between the dilated bile duct and the duodenum. ED was achieved by placing a PVC tube into the dilated bile duct and exteriorizing the other end at the nape of the neck. RESULTS: Minimal adhesions were found around the dilated common bile duct, which made relaparotomy for drainage easy. Alanine transaminase, total bilirubin, alkaline phosphatase, and gamma-glutamyltransferase were significantly raised after bile duct ligation. All parameters returned to control levels after ID for 7 days. In the ED group plasma albumin was significantly decreased and alkaline phosphatase remained marginally elevated. CONCLUSIONS: We have developed a simple and reproducible rat model that allows for the study of reversal of OJ by ID or ED. We also demonstrated that ID is superior to ED in reversing impaired liver function in OJ.     

梗阻性黄疸时脾切除对肠黏膜屏障影响的实验研究

目的 探讨脾脏在梗阻性黄疸(阻黄)中对肠黏膜屏障的作用及其机制.方法 50只Wistar大鼠随机分组,阻黄组开腹结扎胆总管;阻黄+脾切除组,同时切除脾脏.术后7d观察血浆内毒素水平的变化,用乳果糖/甘露醇(L/M)比值检测肠黏膜通透性;采用免疫组织化学、Western印迹检测末端回肠紧密连接蛋白闭锁小带-1(ZO-1)、闭锁蛋白的表达,并利用图像分析系统对Western印迹图像进行定量分析.结果 阻黄+脾切除后L/M的比值和血浆内毒素水平较阻黄组明显下降(均P=0.001).与阻黄组相比,阻黄+脾切除组的平均肠绒毛高度和隐窝深度有所上升(P=0.019、0.001).免疫组化显示术后7 d阻黄组ZO-1蛋白强阳性表达数(6/18)下降明显(P=0.021),阻黄+脾切除组(8/17)染色较阻黄组变化不大;闭锁蛋白的染色阻黄+脾切除组强阳性表达(7/17)高于阻黄组(4/18)(P=0.026).通过对Western印迹图像进行定量分析也得出同样的结论.结论 阻黄后肠黏膜通透性增加,肠黏膜屏障受损.同时切除脾脏,肠紧密连接蛋白成分的数量和分布改变,肠黏膜屏障的损害减轻.

Abstract：

Objective To investigate the effects of splenectomy on the intestine mucosa barrier in rats with obstructive jaundice. Methods 50 Wistar rats were divided randomly into the obstructive jaundice group (OJ), in which the animals underwent operation to ligate common bile duct, and the obstructive jaundice + splenectomy group (OJ+ S). Seven days post-operation, plasma endotoxin levels were detected. Intestinal mucosa permeability was measured by the ratios of lactulose and mannitol (L/M). Immunohistochemistry and Western blot were used to examine the expression of tight junction proteins (ZO-1 and occludin) in the distal ileum mucosa. Western blots images were analyzed quantitatively. Results Average ratios of L/M and plasma endotoxin were decreased obviously in the OJ+S group compared to those in the OJ group (all P=0. 001). Compared with the OJ group, the average intestinal villus height and mucosa thickness were upgraded somewhat in the OJ + S group (P = 0.019, 0. 001 ). By immunohistochemistry staining seven days post-operation, same comment as above the amounts of strong positive expression of ZO-1 were significantly decreased in the OJ group (6/18, P-0. 021). There wewas no difference between the OJ+S group(8/17) and the OJ group.The amount of strong positive expression of occludin was higher in the OJ + S group than that of the OJ group(10/17 vs 4/18, P= 0. 026). The same outcomes were obtained by quantitative Western blot images. Conclusion The intestinal epithelial permeability was increased in rats with obstructive jaundice,and intestinal barrier was damaged. After excising spleen, the amount and distribution of tight junction proteins were changed and the impairment of intestinal barrier was abated.     

梗阻性黄疸时脾切除对肠黏膜屏障影响的实验研究

目的 探讨脾脏在梗阻性黄疸(阻黄)中对肠黏膜屏障的作用及其机制.方法 50只Wistar大鼠随机分组,阻黄组开腹结扎胆总管;阻黄+脾切除组,同时切除脾脏.术后7d观察血浆内毒素水平的变化,用乳果糖/甘露醇(L/M)比值检测肠黏膜通透性;采用免疫组织化学、Western印迹检测末端回肠紧密连接蛋白闭锁小带-1(ZO-1)、闭锁蛋白的表达,并利用图像分析系统对Western印迹图像进行定量分析.结果 阻黄+脾切除后L/M的比值和血浆内毒素水平较阻黄组明显下降(均P=0.001).与阻黄组相比,阻黄+脾切除组的平均肠绒毛高度和隐窝深度有所上升(P=0.019、0.001).免疫组化显示术后7 d阻黄组ZO-1蛋白强阳性表达数(6/18)下降明显(P=0.021),阻黄+脾切除组(8/17)染色较阻黄组变化不大;闭锁蛋白的染色阻黄+脾切除组强阳性表达(7/17)高于阻黄组(4/18)(P=0.026).通过对Western印迹图像进行定量分析也得出同样的结论.结论 阻黄后肠黏膜通透性增加,肠黏膜屏障受损.同时切除脾脏,肠紧密连接蛋白成分的数量和分布改变,肠黏膜屏障的损害减轻.     

Measurement of body water compartments after ligation of the common bile duct in the rabbit

To elucidate the pathogenesis of renal insufficiency associated with obstructive jaundice we have studied spontaneous water intake and body water compartments in rabbits undergoing common bile duct ligation. Total body water, extracellular water and plasma volume were measured by multi-isotope dilution technique. During the initial 6 postoperative days spontaneous water intake was 898 ml in sham operated animals (SO) but only 280 ml in jaundiced rabbits (OJ6) (P less than 0.01). Creatinine clearance was almost unchanged in SO but fell to 60 per cent of the preoperative values both in OJ6 and in paired-drink sham operated animals (SO2). There was a 15 per cent decrease in total body water (P less than 0.01) and a 24 per cent decrease in extracellular water (P less than 0.01) 6 days after bile duct ligation. There was a further reduction of the extracellular water to 35 per cent and a 15 per cent reduction of plasma volume 12 days after ligation. Water restriction mimicked the alterations in body composition produced by bile duct ligation. We conclude that bile duct ligation is associated with hypodypsia and a depletion of extracellular water and plasma volume. These alterations could explain the tendency to develop hypotension and renal failure which are associated with obstructive jaundice.     

诱生型一氧化氮合酶在阻塞性黄疸肝损害中的调控作用

目的：通过体内、外实验，探讨诱生型一氧化氮合酶（iNOS）在阻塞性黄疸肝损害中的调控作用。方法：（1）　体外实验：采用胶原酶原位肝灌注法分离大鼠肝细胞，行原代培养后，用iNOS抑制剂SMT作用于肝细胞，50μmol/L 甘氨鹅脱氧胆酸钠(GCDC) 作用后用流式细胞术（FCM）及原位末端标记法（TUNEL）检测肝细胞凋亡情况。（2）体内实验：结扎大鼠胆总管, 结扎后3，7，14，21d, 分别用TUNEL法及免疫组化SABC法检测大鼠肝组织细胞凋亡状态及iNOS蛋白的表达。结果：（1） 随SMT浓度的增加，肝细胞的凋亡明显减少。（2）大鼠胆总管结扎后随结扎时间的延长细胞凋亡指数(AI)升高，结扎14d后AI达高峰。iNOS蛋白表达越强, 则AI越高。结论：iNOS参与阻塞性黄疸肝细胞凋亡的调节，并在阻塞性黄疸肝损害的发生和发展中起重要作用。     

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.     

Exocrine pancreatic function in obstructive jaundice rats: studies with isolated dispersed pancreatic acini.

This study was conducted to investigate pancreatic exocrine function and pancreatic growth in rats with obstructive jaundice (OJ). OJ was produced in adult male Sprague-Dawley rats by bile duct ligation; control rats underwent laparotomy only. Induction of OJ was associated with significant hyperplasia and hypertrophy of the pancreas in rats as shown by increased DNA and RNA contents of pancreatic tissue. Factors associated with pancreatic growth in OJ rats were further examined in isolated dispersed pancreatic acini from OJ rats and the data were compared with those for control rats. Studies with isolated dispersed acini from OJ rats showed that pancreatic growth was accompanied by significant increases in total cellular amylase content; however, amylase release (percentage of initial) in response to cholecystokinin octapeptide was significantly decreased in OJ rats compared to control rats. Total amylase output in response to 100 pM cholecystokinin (CCK) was higher in the OJ group when compared to the control group (8.6 U/mg protein versus 6.4 U/mg protein), as calculated from the total amylase content and percentage of amylase released. Receptor binding data showed that the capacity of CCK receptors in OJ rats was significantly lower when it was compared with control. In addition, plasma levels of CCK were significantly elevated in OJ rats when compared to controls. These results suggest that obstructive jaundice induces pancreatic growth that is associated with alteration of exocrine pancreatic function. Abnormally high levels of stored amylase in pancreatic acini may be implicated in the development of pancreatitis as often seen in obstructive jaundice patients.     

Effect of Bile Acid Replacement on Endotoxin-induced Tumor Necrosis Factor-a Production in Obstructive Jaundice

There is a high incidence of perioperative morbidity and mortality in patients with obstructive jaundice due to sepsis. Tumor necrosis factor-a (TNF-a) is considered a crucial mediator in inducing and processing the inflammatory cascade. We hypothesize that obstructive jaundice leads to an increased endotoxin-induced TNF-a production and that intestinal bile acid replacement can prevent this phenomenon. Sprague-Dawley rats were randomized to three groups of 12 animals each. Group 1 underwent common bile duct ligation (CBDL) with oral intestinal bile acid (deoxycholic acid 5 mg/100 g body weight/3 times daily) replacement (CBDL + bile acid); group 2 underwent common bile duct ligation with the same amount of normal saline replacement orally (CBDL + saline); and group 3 underwent a sham operation (sham control). After 2 days, endotoxin was given to the animals, and after 90 minutes, tissues (liver and lung) and blood were collected for checking the TNF-a levels and biochemical analyses. Comparisons among these three groups were performed and recorded. While serum and tissue (liver and lung) TNF-a levels of group 2 (CBDL + saline) were significantly increased after endotoxin challenge, these elevations were reduced to control levels (sham control) following oral replacement of intestinal bile acid (CBDL + bile acid). Obstructive jaundice leads to an increased endotoxin-induced TNF-a production and intestinal bile acid replacement can inhibit this phenomenon.     

梗阻性黄疸兔血浆内毒素和内皮素1含量与血流动力学改变的关系

研究梗阻性黄疸内毒素血症对血管内皮细胞产生内皮素１（ＥＴ－１）的作用及ＥＴ－１与梗阻性黄应时血流动力学改变的关系。方法用肝总管结扎法建立梗阻性黄疸（ＯＪ）兔模型,偶氮显色法定量测定血内毒素含量,特异性放射免疫分析法测定血浆ＥＴ－１,生理记录仪和电磁血流计测定心率（ＨＲ）、平均动脉压（ＭＡＰ）、心输出量（ＣＯ）、肝动脉血流量（ＨＡＢＦ）、门静脉血流量（ＰＶＢＦ）、门静脉压力（ＰＶＰ）及内脏血管阻力（ＳＡＲ）。结果ＯＪ组血浆内毒素含量明显高于正常对照（ＮＣ）组;血浆ＥＴ－１低于ＮＣ组。ＯＪ组血浆内毒素与血浆ＥＴ－１含量呈负相关;ＯＪ组血浆ＥＴ－１含量与ＭＡＰ、ＨＡＢＦ、ＰＶＢＦ及ＳＡＲ呈正相关。结论梗阻性黄疽时血浆ＥＴ－１水平降低,内毒素血症不能刺激血管内皮细胞产生ＥＴ－１,血浆ＥＴ－１水平下降在系统血流动力学改变中起一定的作用。