盐酸丁哌卡因硬膜外阻滞对肝酶谱及血浆蛋白参数的影响

应用盐酸丁哌卡因硬膜外阻滞后．测定术毕、术后２４小时印术后一周肝酶谱及血浆蛋白参数动态变比，并与利多卡因进行比较。结果表明：丁哌卡因组（丁组）ＡＬＢ、ＣＰ、ＣＨＥ与术前对照组比较术毕和术后２４小时降低（Ｐ＜０．０１和Ｐ＜０．０５）α－ＡＴ在术毕和术后２４小时增高（Ｐ＜０．０５）。ＡＫＰ和γ－ＣＴ分别在术毕和术后２４小时增高（Ｐ＜０．０５和Ｐ＜０．０１）。术后一周各项指标恢复正常。利多卡因组（利组）仅α－ＡＴ术后２４小时增高（Ｐ＜０．０５）。丁组与利组两组间比较结果：ＣＰ和ＡＤＡ在术毕有显著性差异（Ｐ＜０．０１和Ｐ＜０．０５）。     

原发性肝癌患者可溶性白细胞介素-2受体的变化及其临床意义

对３４例原发性肝癌（ＰＬＣ）患者外周血可溶性白细胞介素－２受体（ｓＩＬ－２Ｒ）、ＮＫ活性、Ｔ淋巴细胞亚群进行测定。结果：ＰＬＣ患者ｓＩＬ－２Ｒ水平明显高于健康对照组（Ｐ＜０．０１），ＮＫ活性、Ｔ淋巴细胞亚群ＣＤ３、ＣＤ４、ＣＤ４／ＣＤ比值均低于正常人（Ｐ＜０．０１），而ＣＤ８高于正常对照组（Ｐ＜０．０５）。Ⅱ、Ⅲ期ＰＬＣ患者ｓＩＬ－２Ｒ水平显著高于Ⅰ期患者（Ｐ＜０．０１）。ｓＩＬ－２Ｒ水平≥１０００ｕ／ｍｌ、５００～１０００ｕ／ｍｌ、＜５００ｕ／ｍｌ者６个月内的死亡率分别为８０．０％、２９．４％、０％。肝癌切除术后２周ｓＩＬ－２Ｒ水平较术前低（Ｐ＜０．０５），免疫治疗后４周ｓＩＬ－２Ｒ水平亦较治疗前低（Ｐ＜０．０５）。细胞免疫水平都有所改善。提示测定外周血ｓＩＬ－２Ｒ水平可作为ＰＬＣ的免疫状态、病情严重程度、疗效观察及预后估计的生物学指标。     

肾肿瘤粘附分子吞噬细胞糖蛋白的测定

为探讨检测肾肿瘤粘附分子吞噬细胞糖蛋白（ＣＤ４４）的方法和临床意义，应用流式细胞免疫学方法，对４８例不同性质及组织学类型的肾肿瘤患者外周血淋巴细胞粘附分子ＣＤ４４及肿瘤组织ＣＤ４４进行测定，并与健康组进行对照。结果：恶性肿瘤组术前淋巴细胞ＣＤ４４阳性率明显高于对照组与良性肿瘤组（Ｐ＜０．０１，Ｐ＜０．０５）；癌细胞ＣＤ４４阳性率高于自身外周血淋巴细胞阳性率（Ｐ＜０．０５）；肾癌不同组织学类型的ＣＤ４４含量差异无显著性；术后外周淋巴细胞ＣＤ４４含量逐渐下降。结论：肾肿瘤组织及外周血淋巴细胞ＣＤ４４检测对鉴别肿瘤性质、早期诊断肿瘤、发现肿瘤复发和转移有重要的临床价值     

山莨菪碱对体外循环心脏手术后白细胞变形力的影响

为观察山莨菪碱对体外循环（ＣＰＢ）心脏手术后病人白细胞变形能力（ＬＤ）的影响，进一步探讨该药改善微循环的机制。将１６例体外循环下心脏手术病人均分为实验、对照组。实验组于术后６０分钟静脉注射山莨菪碱０．２ｍｇ／ｋｇ。两组分别于术前、术后６０、给药后３０、６０分钟采外周血，测定白细胞变形力。结果显示，ＣＰＢ术后６０分钟两组白细胞变形力均明显降低（Ｐ＜０．０１），组间差异无显著性（Ｐ＞０．０５）。实验组给药后３０分钟ＬＤ高于对照组（Ｐ＜０．０１），但两组仍低于术前（Ｐ＜０．０１），给药后６０分钟实验组ＬＤ恢复至术前水平（Ｐ＞０．０５），明显高于对照组（Ｐ＜０．０１）。结论：ＣＰＢ术后ＬＤ降低，山莨菪碱对微循环的改善除作用于血管平滑肌及内皮外，提高ＬＤ亦起着重要作用     

梗阻性黄疸患者的内毒素血症及其对机体的影响

４９例梗阻性黄疸（梗黄）患者（实验组）和８１例无黄疸胆系疾病患者（对照组）围手术期外周血的内毒素（ＥＴ）检测结果表明，实验组：①术前ＥＴ阳性率明显高于对照组（Ｐ＜０．００１）；②术后１０～１２天夹闭Ｔ／Ｙ管后ＥＴ阳性率明显低于术前和夹管前（Ｐ＜０．００１）；③伴急性化脓性胆管炎（ＡＣＳＴ）的患者ＥＴ阳性率明显高于无ＡＣＳＴ的患者（Ｐ＜０．００１）。作者认为，本组梗黄患者中出现的肾功能障碍、胃肠道出血以及２例患者的死亡，可能部分与内毒素血症有关。     

肝硬变门脉高压症及不同术式对大鼠肝脏储备功能的影响

用四氯化碳／乙醇诱导的大鼠肝硬变模型分为４组：①选择性远端脾腔分流术（ＤＳＣＳ）；②门奇断流术（ＰＡＤ）；③肠腔侧侧分流术（ＭＣＳ）和④肝硬变组。在术后１、３、５周进行口服糖耐量试验（ＯＧＴＴ）、胰高糖素负荷试验（ＧＬＴ），比较各组肝脏储备功能的变化。结果表明：术后第１周ＤＳＣＳ、ＰＡＤ和ＭＣＳ与肝硬变组比较无显著性差异（Ｐ＞０．０５）；而术后第３和５周，ＤＳＣＳ和ＰＡＤ组与肝硬变组比较有显著性差异（Ｐ＜０．０５），ＭＣＳ组与肝硬变组比较无显著性差异（Ｐ＞０．０５）。本研究结果表明：ＤＳＣＳ和ＰＡＤ组大鼠肝脏储备功能明显优于ＭＣＳ组和肝硬变组。     

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     

胆酸钠、乳果糖、山莨菪碱对梗阻性黄疸内毒素血症的临床治疗观察

目的 观察术前３种药物对梗阻性黄疸（简称：梗黄）病人抗内毒素血症的治疗作用。方法 ４８例梗黄病人分４组在术前分别给予一般治疗（Ａ组）,口服胆酸钠（Ｂ组）。口服乳果糖（Ｃ组）和静脉滴注山莨菪碱（Ｄ组）处理,和２１例无黄疸病人进行手术前后内毒素（ＥＴ）含量测定。结果 （１）入院时梗黄各组外周血ＥＴ水平差异无显著意义（Ｐ〉０．０５）,但均显著高于无黄疸组（Ｐ〈０．０１）;（２）Ａ组门静脉血ＥＴ水平明显高于外周血（Ｐ〈０．０５）;Ａ组手术后５ｄＥＴ水平降低不明显随后ＥＴ逐渐下降,ｄ１５接近正常水平;（３）Ｂ,Ｃ２组用药后外周血ＥＴ水平明显下降,术后ＥＴ水平继续降低,Ｂ,Ｃ２组门静脉血ＥＴ水平低于Ａ组（Ｐ〈０．０５）;（４）Ｄ组用药后外周血和术中门静脉血ＥＴ水平明显低于Ａ组（Ｐ〈０．０５）。术后也保持低水平。结论 术前应     

心脏手术中小剂量抑肽酶对中性粒细胞CD_(11b)/CD_(18)表达的影响

目的 探讨体外循环术（ＣＰＢ）中小剂量抑肽酶对全身炎性反应的抑制作用。方法２８例首次行心脏瓣膜置换术患者随机分为对照组和抑肽酶组,各１４例,于麻醉诱导前、ＣＰＢ前、ＣＰＢ结束后１ｈ及２４ｈ用免疫流式细胞仪分别测定中性粒细胞表面粘附分子ＣＤ１１ｂ和ＣＤ１８的表达。结果ＣＤ１１ｂ／ＣＤ１８的表达与ＣＰＢ时间呈正相关（相关系数γ分别为０．６４４、０．５３８,Ｐ＜０．０５）,ＣＰＢ结束后１ｈ及２４ｈ对照组ＣＤ１１ｂ的表达较麻醉诱导前及同时点的抑肽酶组明显上调（Ｐ＜０．０５）;ＣＤ１８的表达仅在ＣＰＢ结束后１ｈ明显上调并高于抑肽酶组（Ｐ＜０．０５）,ＣＰＢ结束后２４ｈ表达下凋有所缓解,但仍高于麻醉前基础值（Ｐ＜０．０５）。结论 ＣＰＢ所致的炎性反应可能与转机时间有关,小剂量抑肽酶对ＣＰＢ术后ＣＤ１１ｂ／ＣＤ１８表达增加具有抑制作用。     

早期肠道营养对烧伤后肠道功能的维护

选择平均烧伤面积４５％成人２１例，随机分为早期喂养（ＥＦ组）和延迟喂养组（ＤＦ组），探讨早期肠道营养对严重烧伤病人肠道功能的维护作用。结果表明内毒素在伤后４，８天ＥＦ组显著低于ＤＦ组（Ｐ＜０．０５～０．０１）；而ＳＯＤ则呈相反的变化，在伤后４，８天ＥＦ组显著高于ＤＦ组（Ｐ＜０．０１）；胃泌素和胃动素除伤后第１天的大多时相点ＥＦ组显著高于ＤＦ组（Ｐ＜０．０５～０．０１），而炎症介质ＴＮＦ和ＩＬ－８则呈相反的变化，两组间差异有显著意义（Ｐ＜０．０５～０．０１）。提示早期肠道营养可降低循环内毒素水平，减轻肠道缺血性再灌注损伤，削弱、阻滞“内毒素——炎症介质”对肠粘膜的损伤     

Expression of intercellular adhesion molecule-1 (ICAM-1) during hypoxia-reoxygenation by sinusoidal endothelial cells (SECs) in an obstructive jaundice model

Background/Purpose: The aim of the present study was to investigate the expression of intercellular adhesion molecule-1 (ICAM-1) by sinusoidal endothelial cells (SECs) during hypoxia-reoxygenation in an obstructive jaundice model. Methods: Male Wistar rats aged 6 to 8 weeks were assigned to an obstructive jaundice group (group OJ; n= 8) and a sham-operated control group (group S; n= 8). Using flow cytometry, we determined the percentage of ICAM-1-positive cells and the mean fluorescence intensity (MFI) of ICAM-1 per cell in each group during hypoxia-reoxygenation. Results: The percentage of ICAM-1-positive cells in group OJ did not change significantly under successive incubation conditions. However, the MFI in group OJ differed significantly between normoxia and 24-h renormoxia. The present study investigated the function of isolated SECs from rats with obstructive jaundice and hypoxia-reoxygenation. The percentage of ICAM-1-positive cells and the MFI of ICAM-1-positive cells showed quite similar changes caused by hypoxia-reoxygenation stress in group S and Group OJ. The ICAM-1 expression increased with hypoxia-reoxygenation in both normal and OJ SECs, and the amount of ICAM-1, on the whole, increased. Obstructive jaundice increased the percentage of ICAM-1-positive cells from the normal state. Conclusions: The amount of ICAM-1 increased with hypoxia-reoxygenation in obstructive jaundice than normal state. Received: July 13, 2001 / Accepted: November 16, 2001     

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。     

不同引流方式对恶性梗阻性黄疸患者细胞免疫的影响

目的探讨高位梗阻内镜下逆行胰胆管造影术(ERCP)内引流和经皮经肝胆管引流术(PTCD)内引流,以及低位梗阻ERCP内引流和开腹胆肠吻合手术对恶性阻塞性黄疸患者细胞免疫力的影响。方法 选择恶性梗阻性黄疸患者120例,采用抽样分层的方法 ,根据高位和低位梗阻随机分为四组,分别采用不同引流方式治疗,于术前一天和术后第1天、第1周以及第2周抽空腹静脉血,检测血清中脂多糖(LPS)含量、可溶性白介素-2受体(sIL-2R)浓度以及血液中CD8+CD28-T细胞含量,比较患者细胞免疫的变化情况。以正常志愿献血者30例作为对照组。结果四组患者术前血清中LPS含量、sIL-2R浓度以及血液中CD8+CD28-T细胞含量均明显高于对照组;术后2周,四组患者均较术前明显下降(P0.05),但仍较对照组高(P0.05),ERCP组较其他两组下降最明显(P0.05)。结论恶性梗阻性黄疸患者细胞免疫力下降;经ERCP下胆道内支架引流治疗的患者免疫力恢复最快。     

梗阻性黄疸时胆道内压力和门静脉血流与IL-2、sIL-2R及T淋巴细胞亚群变化的关系探讨

为探讨梗阻性黄疸患者败血症的发生机理，研究了３７例梗阻性黄疸（Ａ组）和９０例胆囊结石（Ｂ组）患者的胆道内压力、门静脉血流速度与白细胞介素－２（ＩＬ－２）、可溶性白细胞介素－２受体（ｓＩＬ－２Ｒ）及Ｔ淋巴细胞亚群的关系。Ａ组又分为急诊手术组（Ａ１）、择期手术组（Ａ２）、＞６０岁组（Ａ３）和＜６０岁组（Ａ４）４个亚组。结果显示：Ａ及Ａ１～４各组术前ＣＤ３＋、ＣＤ４＋、ＣＤ８＋值均显著低于术后１０天值（Ｐ＜０．０５或Ｐ＜０．０１），ｓＩＬ－２Ｒ显著高于术后１０天值（Ｐ＜０．０１）。Ａ１组术前ｓＩＬ－２Ｒ极显著高于Ａ及Ａ２～４组（Ｐ＜０．０１）。相关分析显示胆道内压力与ＩＬ－２、ＣＤ３＋、ＣＤ４＋及ＣＤ８＋呈负相关，与ｓＩＬ－２Ｒ呈正相关（Ｐ＜０．０１），门静脉血流速度与ＩＬ－２呈正相关（Ｐ＜０．０１）。由此表明梗阻性黄疸感染与宿主细胞免疫功能降低密切相关。     

阻塞性黄疸时肠粘膜免疫功能变化的实验研究

阻塞性黄疸(阻黄)病人机体免疫功能受到抑制。本实验目的是研究阻黄时肠粘膜免疫功能的改变。实验包括阻黄组和对照组,采用胆总管结扎制造阻黄模型,以胆汁外引流组作为对照,每组15只动物。制造阻黄模型后2周,取小肠检测肠液中分泌型IgA(S-IgA)浓度、肠粘膜内淋巴细胞体外刺激转化能力、粘膜固有层内淋巴细胞亚群。结果显示:与对照组相比,阻黄鼠肠液S-IgA浓度降低;肠粘膜内淋巴细胞刺激转化能力降低;粘膜固有层内含IgA浆细胞、CD4阳性和CD8阳性淋巴细胞数目减少,差别有显著性(P>0.05)。因此,我们认为阻黄时肠粘膜免疫功能受到明显抑制。     

恶性重度梗阻性黄疸对机体免疫功能的影响及免疫增强剂的治疗作用

目的 探讨恶性重度梗阻性黄疸对机体免疫功能的影响及免疫增强剂的治疗作用。方法 选择我院2010年3月至2012年7月收治的无明显黄疸（TBil＜17.1μmol/L）的胆石症患者（A组,无黄疸对照组,n=20）,恶性非重度梗阻性黄疸患者（TBil17.1～342μmol/L）（B组,恶性非重度黄疸组,n=20）,恶性重度梗阻性黄疸（TBil＞342μmol/L）行经皮经肝穿刺胆管引流术（PTCD）患者（C组,恶性重度黄疸组,n=39）。其中C组又分成免疫增强剂治疗组（C1,n=18）和非治疗组（C2,n=21）。C1组PTCD术后当天开始给予注射用胸腺肽α-1,1.6 mg/d,皮下注射,连用7 d。比较各组血浆细胞因子（IL-2、IFN-α、TNF-α）、T淋巴细胞亚群（CD3+、CD4+、CD8+）和NK细胞百分率的变化。结果 C组CD3+、CD4+、CD8+、NK细胞百分率及IL-2明显低于A组（P＜0.05）,CD3+、CD8+百分率及IL-2明显低于B组（P＜0.05）;TNF-α、IFN-αC组明显高于A组和B组（P＜0.05）;B组CD3+、NK细胞百分率及IL-2明显低于A组（P＜0.05）;CD4+/CD8+比值各组间无明显差异。C1组CD3+、CD4+百分率,CD4+/CD8+比值及IL-2呈升高趋势,TNF-α、IFN-α呈降低趋势,胸腺肽α-1治疗后第5天CD3+、CD4+百分率明显高于C2组（P＜0.05）,第7天CD4+百分率、CD4+/CD8+比值、IL-2、IFN-α明显高于C2组（P＜0.05）,TNF-α明显低于C2组（P＜0.05）。结论 恶性梗阻性黄疸患者免疫功能降低,重度黄疸时免疫功能受损更加明显。免疫增强剂可明显改善恶性梗阻性黄疸患者的免疫功能。     

七氟醚麻醉中阻塞性黄疸患者的血流动力学变化

目的 探讨阻塞性黄疸患者在七氟醚吸入麻醉过程中血流动力学的变化.方法 择期手术患者80例,ASA Ⅰ或Ⅱ级,按照血清总胆红素(sTBL)水平分为观察组(A组,sTBL≥17.1μmol/L)和对照组(B组,sTBL<17.1 μmol/L),每组40例.分别在麻醉诱导前、呼出气七氟醚浓度在1.0 MAC和1.5 MAC并维持10 min时记录血流动力学指标.结果 麻醉诱导前A组MAP、HR、全身血管阻力(SVR)、心脏指数(CI)、肺毛细血管楔压(PCWP)明显低于B组(P<0.05或P<0.01).1.0 MAC时A组MAP、平均肺动脉压(MPAP)、CI、每搏指数(SI)的下降百分率均明显大于B组(P<0.05或P<0.01).1.5MAC时A组患者MPAP、MAP、CI的下降百分率明显大于B组(P<0.05或P<0.01).结论 与非阻塞性黄疸患者比较,阻塞性黄疸患者血流动力学随七氟醚呼出气浓度增加而波动增大.     

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 N-acetylcysteine on blood and tissue lipid peroxidation in lipopolysaccharide-induced obstructive jaundice.

In obstructive jaundice, free radical production is increased and antioxidative activity is reduced. N-Acetylcysteine (NAC) has a beneficial effect with anti-inflammatory and antioxidant activity, acting as a free radical scavenger. NAC inhibits inducible nitric oxide synthase, suppresses cytokine expression/release, and inhibits adhesion molecule expression and nuclear factor kappa B. The aim of this study was to investigate the effects of NAC on liver/renal tissue and serum lipid peroxidation in lipopolysaccharide (LPS)-induced obstructive jaundice. We randomized 60 rats into 6 groups: group 1, Sham; group 2, obstructive jaundice (OJ) induced after bile-duct ligation; group 3, OJ + NAC (100 mg kg- 1 subcutaneously); group 4, OJ + LPS (10 mg kg-1); group 5, OJ + NAC + LPS; and group 6, OJ + LPS + NAC. For each group, the biochemical markers of lipid peroxidation and the antioxidant products were measured in serum and liver/renal tissue after sacrifice. Almost all lipid peroxidation products levels were increased and antioxidant products levels were decreased in groups who received LPS (groups 4, 5, and 6), but the effect was less remarkable when NAC was administered before LPS (group 5). The same trend was seen for groups with OJ +/- LPS who did not received NAC or received it after induced toxemia (groups 2, 4, and 6) as compared to groups 1 and 3. Moreover, in the case of OJ + LPS, rats treated with NAC before LPS (group 5) had lower lipid peroxidation products levels and higher antioxidant products levels as compared to those who did not received NAC (group 4). This phenomenon was not reproducible with NAC administered after LPS (group 6). Thus, results of this study showed that NAC prevents the deleterious effects of LPS in obstructive jaundice by reducing lipid peroxidation in serum and liver/renal tissue if administered before LPS. Nonetheless, NAC failed to prevent the lipid peroxidation in the case of established endotoxemia in obstructive jaundice.