大鼠肝硬化门静脉高压形成过程中内皮素A受体mRNA的表达

目的：观察Wistar大鼠肝硬化门静脉高压形成过程中内皮素A受体（ETA）mRNA在肝脏中的表达,探讨内皮素（ET）及其受体对肝硬化门静脉高压大鼠肝脏的调节机制。方法：CCL4法制备模型。实验共分4组：正常对照组（13只）、肝细胞变性坏死期组（20只）、肝细胞结节状增生期组（20只）、假小叶形成期组（18只）。应用mRNA原位杂交技术确定ETA的部位,从而发现ET在肝脏的作用位点,并对ETAmRNA进行定量分析。结果：Wistar大鼠肝硬化门静脉高压形成过程中,肝脏发生特征性病理改变：肝细胞变性坏死、结节状增生、假小叶形成;门静脉压力呈梯度性升高;外周及门静脉血浆ET水平随门静脉压力升高而降低;肝脏ETAmRNA表达增多,表达主要位于汇管区门静脉小静脉、肝小动脉血管壁,小静脉表达明显高于小动脉,表达水平随ET浓度的降低、门静脉压力的升高而增加。结论：大鼠肝硬化门静脉高压形成过程中外周及门静脉血浆ET水平进行性降低;肝脏微循环ETAmRNA表达量增加,呈现上调趋势;表达部位随肝硬化进展发生特征性变化。     

内皮素-1对门静脉高压大鼠胃黏膜微循环的调节机制

目的：检测内皮素A受体（endothelin A receptor,ETA）mRNA在胃黏膜微循环血管上的表达位点,探讨内皮素-1（ET-1）对肝硬化门静脉高压大鼠胃黏膜微循环的调节机制.方法：用60?L4（0.3 ml/100 g体重）皮下注射方法制作大鼠肝硬化门静脉高压性胃病模型.实验共分4组：正常对照组（n=13）、肝细胞变性坏死期组（n=20）、肝细胞结节状增生期组（n=20）和假小叶形成期组（n=18）.应用mRNA原位杂交技术确定ETA受体的表达部位,以能发现ET-1在胃黏膜微循环血管壁的作用位点,并测定实验大鼠门静脉压力、外周及门静脉血ET水平,以动态观察肝硬化门静脉高压形成过程中门静脉压力、门静脉与外周血ET水平变化及其规律.结果：Wistar大鼠在肝硬化门静脉高压形成过程中,其胃黏膜厚度增加,黏膜淤血;门静脉压力呈梯度性升高;外周及门静脉血浆ET水平随门静脉压力升高而降低;胃黏膜ETA mRNA主要在黏膜基底部的微循环前微动脉和后微静脉血管壁表达,其表达水平随ET浓度的降低和门静脉压力的升高而增加,且其在小动脉表达明显强于小静脉.结论：大鼠在肝硬化门静脉高压形成过程中,其外周及门静脉血浆ET水平呈进行性降低;胃黏膜微循环血管壁中的ETA mRNA表达量增加,呈现上调趋势;ET及其受体mRNA表达的这种变化可能与肝硬化门静脉高压大鼠胃黏膜微循环功能障碍有关.     

内皮素在肝外型门静脉高压症发病机制中的作用

目的 探讨内皮素在门静脉高压症发病机制中的作用及其可能的机制。方法 参照Benoit方法建立大鼠门静脉高压症模型,应用放射免疫学方法分别测定门静脉高压症组、正常对照组和假手术组大鼠血浆及肝组织中ET－1的含量,并观察ET－1和ETA受体拮抗剂对门静脉高压症大鼠FPP以及体外培养的门静脉血管平滑肌细胞（VSMC）增殖和蛋白质合成的影响。结果 ①门静脉高压症大鼠血浆和肝组织ET－1含量显著高于正常对照组和假手术组（P＜0．01）;②静脉注ET－1可以显著提高门静脉高压症大鼠的自由门静脉压（P＝0．002）,静注ETA受体拮抗剂则可以显著降低门静脉高压症大鼠的FPP（P＝0．047）;③ET－1可以显著剂量依赖性地促进门静静脉VSMC对^3H-TdR和^3H-Leu的掺入,这种作用可以被ETA受体拮抗剂所抑制。结论 ①ET－1可以通过ETA受体介民垢缩血管作用,增加肝内门静脉系统血流阻力的功能性部分;②ET－1可以显著促进体外培养的大鼠门静脉血管平滑肌细胞的增殖和蛋白质合成,参与门静脉系统的血管增生－血管重构,并影响门静脉系统血流阻力的器质性部分;③门静脉高压症大鼠体内ET－1的过量表达通过影响门静脉系统血流阻力的功能性部分和器质性部分,在门静脉高压症的发病机理中具有重要作用。     

一氧化氮合酶、内皮素在门脉高压大鼠肠粘膜中的表达变化

目的　探讨一氧化氮合酶和内皮素 -1在门脉高压大鼠肠粘膜中的表达情况。方法　2 0只雄性SD大鼠随机分为实验组与对照组 ,实验组行门静脉两步结扎加左肾上腺静脉结扎 ;应用免疫组化SP染色法检测iNOS、ecNOS及ET -1在大鼠小肠和结肠粘膜中的表达情况。结果　门静脉完全结扎后两周 ,实验组大鼠门静脉压力较对照组明显增高 ;iNOS、ecNOS及ET -1在小肠粘膜中表达强度较对照组增强 ,iNOS及ET -1在结肠粘膜中表达较对照组增强。结论　门脉高压大鼠小肠、结肠粘膜局部病变中iNOS、ecNOS及ET -1的表达不完全一致     

内毒素耐受对脓毒症大鼠肠道功能的保护作用

目的：动态观察内毒素耐受大鼠在内毒素血症时肠道炎症反应和免疫功能的变化,探讨内毒素耐受对内毒素血症大鼠肠道的保护作用及其机制。方法：选择健康成年雄性SD大鼠70只,随机分成3组：正常对照组（10只）、内毒素（LPS）组（30只）和内毒素耐受组（30只）。内毒素耐受组大鼠于实验第1日经腹腔注射LPS 0.25 mg/kg,24h后经腹腔注射LPS 0.5 mg/kg,LPS组在上述时间均给予等量生理盐水;实验第5日上述两组大鼠均腹腔注射大剂量LPS 10 mg/kg,于注射大剂量LPS前（0h）和注射后2、4、6、12h取大鼠肠组织制备肠黏膜上清液,用双抗体夹心法测定肠黏膜组织中分泌型免疫球蛋白A（sIgA）的含量,用免疫组化技术检测肠组织细胞间黏附分子-1（ICAM-1）的表达,并与正常对照组进行比较;光学显微镜下观察3组大鼠肠组织病理学变化,并进行病理学评分。结果：内毒素耐受组在给予小剂量LPS后没有出现体重下降。内毒素耐受组肠黏膜中slgA的含量较正常对照组明显升高,6 h最为明显（P〈0.05）,LPS组sIgA含量2 h明显升高（P〈0.05）,从6 h开始下降（P〈0.05）。内毒素耐受组给予大剂量LPS后肠黏膜ICAM-1的表达没有呈上升趋势,各时间点ICAM-1的表达与正常对照组比较差异有显著性,以6h ICAM-1的表达最低,而LPS组肠黏膜ICAM-1的表达随时间的延长逐渐升高,明显高于内毒素耐受组。肠组织病理学观察可见：LPS组肠黏膜水肿,绒毛脱落,并伴有大量炎性细胞浸润;内毒素耐受组上述表现较LPS组减轻。两组肠黏膜炎症损伤病理学评分[LPS组（3.89±0.45）分;内毒素耐受组（2.65±0.36）分]差异有显著性（P〈0.01）。结论：内毒素耐受可减轻内毒素血症导致的肠道黏膜屏障的损害,升高sIgA水平,减少ICAM-1表达,从而起到肠保护作用。     

门静脉高压形成中内源性硫化氢体系的变化及其对一氧化氮/一氧化氮合酶途径的影响

目的 研究新型气体信号分子硫化氢(hydrogen sulfide,H2S)在大鼠门静脉高压形成中的作用以及对内源性一氧化氮(nitric oxide,NO)/一氧化氮合酶(nitric oxide synthase,NOS)体系的调节作用,以深入探讨H2S在大鼠门静脉高压形成中的病理生理意义.方法 将30只健康SD大鼠随机分为4组:正常组(5只),假手术组(5只),部分门静脉结扎(partly portal vein ligation,PPVL)组(10只)及PPVL+NaHS组(10只).模型制作14 d后,分别测定各组大鼠的门静脉压力(portal venous pressure,PVP)和平均动脉压力(systemic mean arterial pressure,MAP);采用免疫组织化学方法榆测大鼠肝脏中胱硫醚-γ-裂解酶(cystathionine-γ-lyase,CSE)和NOS蛋白表达情况,RT-PCR方法检测肝脏中CSE和NOS mRNA表达情况.结果 术后14 d,假手术组和正常组各项检测指标未见显著差异.与正常组比较,PPVL组PVP明显增高(P＜0.01),MAP下降(P＜0.05);外源件给予H2S的供体-NaHS后,与PPVL组比较,PPVL+ NaHS组PVP进一步增高(P＜0.05),MAP进一步下降(P＜0.05).CSE、NOS3在各组大鼠的肝脏中均有表达.与正常组比较,PPVL组CSE蛋白及mRNA表达增加(P＜0.05);外源性给予NaHS后,其表达则进一步增加(P＜0.05).NOS2在正常组和假手术组未见明显表达,部分门静脉结扎后,大鼠肝脏中可见NOS2蛋白及mRNA表达,外源性给予NaHS后,其表达降低(P＜0.05).但是,NOS3蛋白及mRNA表达在各组之间无显著差异.结论 H2S参与了门静脉高压的形成与发展,外源性给予NaHS可以加重门静脉高压,内源性H2S的高水平可以抑制NOS的生成.     

门静脉动脉化治疗门静脉高压症的实验研究

目的观察门静脉动脉化 完全门体分流(PACS)术和传统的脾肾分流(SRS)术及贲门周围血管离断(PCDV)术对门静脉血流动力学的影响。方法制备门静脉高压动物模型,PCDV组行脾切除、贲门周围血管离断术;SRS组采用脾切除、远端脾肾分流术;PACS组采用脾切除、门静脉-脾动脉吻合、门静脉-腔静脉吻合。应用彩色多普勒超声及有创性测压管于开腹后即刻、手术完成即刻及治疗后2周测量门静脉血流量(PVF)及门静脉压力(PVP),PACS组包括入肝及入下腔静脉PVF、PVP。手术前、后测定肝功能指标。结果PCDV组术后2周PVF下降约17%,PVP下降约5%;SRS组术后2周PVF下降约51%,PVP下降约51%;PACS组术后2周入肝PVF上升至开腹后即刻的180%,入肝PVP上升至开腹后即刻的196%,入下腔静脉PVF增至开腹后即刻的130%,入下腔静脉PVP保持低压,约为开腹后即刻的46%。术后2周PACS组入肝PVP、PVF及入下腔静脉PVF均明显高于另2组(P<0.05,P<0.01),而入下腔静脉PVP则明显低于PCDV组(P<0.05)。3组中仅SRS组术后2周ALT较术前明显升高(P<0.05)。结论PACS术成功率较高,手术死亡率与SRS术相近,可同时提高入肝血流和降低侧支压力,而且短期内未明显影响肝脏功能,是一种值得尝试和进一步研究的新手术方法。     

乌司他丁对脓毒症急性肾损伤大鼠肾脏NOD1受体和血IL-18水平的影响

目的 探讨乌司他丁对腹主动脉阻断联合腹腔注射脂多糖内毒素（LPS）构建严重脓毒症大鼠肾脏NOD1受体表达和血IL-18水平的影响.方法 48只Wistar大鼠随机分为假手术组（SHAM组）、腹主动脉阻断联合腹腔注射LPS组（AAC＋ LPS组）、腹主动脉阻断联合腹腔注射LPS乌司他丁干预组（AAC＋ LPS＋U组）、腹主动脉阻断腹腔LPS生理盐水对照组（AAC＋ LPS＋ NS组）.大鼠于术后或干预后8h处死,收集血和大鼠肾脏,检测血中Cr、BUN水平,ELISA方法检测血中IL-18浓度,免疫组化方法检测肾脏NOD1蛋白的表达,RT-PCR方法检测肾脏NOD1 mRNA的表达.结果 NOD1受体mRNA和蛋白的表达,血中IL-18和Cr、BUN水平在AAC ＋LPS组和AAC＋LPS ＋NS组最强,AAC＋ LPS＋U组较前两组下降,差异有统计学意义（P＜0.05）.结论 乌司他丁可能通过抑制肾脏NOD1受体的表达,抑制血中IL-18的分泌从而在脓毒症时发挥抗炎和肾脏保护作用.     

PEG-CAT改善门静脉高压症全身高动力循环的实验探索

目的 研究聚乙二醇过氧化氢酶（polyethylene glycol-catalase,PEG-CAT）对肝硬化门静脉高压症大鼠脏器血流动力学的影响,并探明活性氧产物在肝硬化门静脉高压症治疗中的作用。方法 实验分为正常大鼠（正常组,共6只）、CCl4诱导的肝硬化门静脉高压症大鼠（门静脉高压组,共7只）以及PEG-CAT处理的门静脉高压症大鼠（PEG-CAT组,共6只）。采用插管法测动脉及门静脉压力,彩色微球法检测心出量及内脏器官血流变化,过氧化氢检测试剂盒检测小肠及肠系膜过氧化氢含量变化,并用Western blotting 测小肠及肠系膜血管形成标志物VEGF、VEGFR2及CD31蛋白表达。结果 （1）门静脉压力：与正常组比,门静 脉高压组和PEG-CAT组明显升高（P＜0.05）,但后两组差异无统计学意义（P＞0.05）;（2）脏器血流：与正常组比,除胰腺及结肠血流无明显差别外（P＞0.05）,实验组其他各内脏血流均显著升高（P＜0.05）,PEG-CAT干预则能显著降低上述各内脏血流量;（3）过氧化氢含量：与正常组比,门静脉高压组小肠及肠系膜中过氧化氢含量显著升高（P＜0.05）,在PEG-CAT干预后其含量显著降低（P＜0.05）,但与正常组比无统计学差异（P＞0.05）;（4）使用PEG-CAT降低组织过氧化氢含量后,VEGF、VEGFR2及CD31三种蛋白表达均显著降低（P＜0.05）。结论 CCl4致肝硬化门静脉高压症大鼠小肠及肠系膜过氧化氢含量增高,从而导致VEGF、 VEGFR2及CD31蛋白表达增加及门静脉血流阻力减少和血流量增加。PEG-CAT干预虽不能降低门静脉压力,但可显著降低门静脉血流量。这一实验结果肯定了过氧化氢在肝硬化门静脉高压症内脏高血液动力状态形成 中的作用,并为以降低内脏组织过氧化氢含量为宗旨的肝硬化门静脉高压症临床治疗提供了初步实验依据。     

大鼠体外循环后肝脏生长激素受体mRNA的变化及其意义

目的 探讨大鼠体外循环（CPB）后肝脏生长激素受体mRNA（GHRmRNA）的变化及意义。方法 建立大鼠CPB模型,按照CPB后不同时间进行分组,检测血清生长激素（GH）、生长激素结合蛋白（GHBP）、内毒素（LPS）、白细胞介素6（IL-6）、前白蛋白（PA）水平及肝功能。RT-PCR法检测肝组织GHRmRNA。结果 CPB1．0h后肝功能损害明显,LPS、IL-6开始升高,CPB结束后2．0h达到峰值;GH、GHBP、GHRmRNA变化趋势与之相反,并与黄疸程度、LPS、IL-6水平呈负相关（P〈0．01）、与PA呈正相关（P〈0．01）。结论 CPB术后早期肝功能已受到损害,GH／GHR轴存在明显下调,其原因可能与内毒素血症引起的生长激素受体表达受抑有关;并可进一步加重炎症反应,是介导CPB肝脏病理生理改变的重要因素。     

一氧化氮在大鼠肝硬变门静脉高压症形成中的作用及其对血液动力学 …

目的 探讨一氧化氮（ＮＯ）在肝硬变门静脉高压症（ＰＨＴ）形成过程中的作用。方法 采用比色法和鲎试验改良基质显色法,对大鼠肝硬变ＰＨＴ形成过程中,外周血ＮＯ、内毒素浓度和血液动力学的变化进行检测,观察了ＮＯ合成酶抑制剂Ｌ－ＮＭＭＡ对ＰＨＴ大鼠血液动力学的影响。 结果 （１）在大鼠肝硬变ＰＨＴ形成过程的早、中、晚三期,血浆ＮＯ和内毒素水平显著升高。（２）在肝硬变形成各期门静脉阻力（ＰＶＲ）和门静脉压力     

Enhancement of portal blood flow by ursodesoxycholic acid in partially hepatectomized rats

Portal venous flow (PVF) was examined after portal injection of ursodesoxycholic acid (URSO) in rats that were partially hepatectomized by either 40% or 66%. URSO (10 mg/kg per minute) was injected into the portal vein and was thereafter observed to increase PVF concomitantly with a fall in portal venous pressure (PVP) in control animals. The increase in PVF in response to URSO was dose-dependent. In hepatectomized rats, the PVF response was augmented when the same dose of URSO was portally injected, and the magnitude of response was enhanced in proportion to the volume of liver resected. These results suggest that URSO increases PVF through vasodilation of the portal vessels, and therefore URSO is considered to increase PVF potently in a partially hepatectomized condition.     

CO2气腹对肝硬变大鼠门脉血流影响的实验研究

目的　探讨CO2 气腹对肝硬变大鼠门脉血流量的影响。　方法　制作肝硬变大鼠模型 ,施加不同压力的气腹 ,分别测平均动脉压、门静脉压力、下腔静脉压、门静脉血流 ,计算门静脉阻力。　结果　平均动脉压、下腔静脉压在不同气腹压力下无明显变化 ,两组大鼠门静脉压力在 10mmHg时出现显著差异 ,随着压力的升高而升高。正常大鼠的门静脉血流量在 2 0mmHg下与 0mmHg下比较有显著差异 ,而肝硬变大鼠的门静脉血流量在 10mmHg下与 0mmHg下比较已有显著差异。正常大鼠门静脉阻力随着压力的升高在 10mmHg时出现显著差异 ,以后继续升高 ,肝硬化大鼠门静脉阻力随着压力的升高持续升高。　结论　CO2 气腹致肝硬化大鼠门静脉血流减少 ,且减少程度重于正常大鼠     

A pharmacological analysis of prostaglandin E1 on portal blood flow after partial hepatectomy in rats

Portal venous flow (PVF) and portal venous pressure (PVP) were examined after the jugular or portal injection of Prostaglandin E₁ (PGE) in rats partially hepatectomized by either 40% or 66%. In the 66% hepatectomized animals, the jugular injection of PGE at 5.0 g/kg/min produced an increase in PVF concomitant with a fall in systemic arterial pressure (SAP), while PVP remained unchanged. The portal injection of PGE at 0.5 g/kg/min increased PVF to a level equivalent to that evoked by the jugular injection of 5.0 g/kg/min PGE, without any change in SAP. PVP was reduced synchronistically with an increase in PVF. The PVF response to a portal injection of PGE at 0.5 g/kg/min was not reproduced in liver intact rats. These results suggest that PGE is potent in increasing PVF in the partially resected condition of the liver and that the portal vascular bed is involved in this response.     

一氧化氮、内皮素-1在内毒质所致肝脏损伤中的作用机制研究

目的 探讨一氧化氮（NO）和内皮素-1（ET-1）在内毒素所致肝脏损伤中的作用机制。方法 Waster大鼠40只随机分成对照组，内毒素组、内毒素组、内皮素受体拮抗剂组和左旋精氨酸组，观察各组大鼠血浆NO和ET-1水平，肝脏功能变化，在光镜下观察肝细胞损伤程度，在电镜下观察肝脏超微结构改变。结果 大鼠投予内毒素12h后，血浆NO和ET-1水平明显下升，血浆转氨酶水平增加，肝细胞明显水肿，变性和坏死，肝筛的数量和直径明显减少，左旋精氨酸和内皮素受体损坏抗剂均能明显减轻肝脏功能和结构的损伤，结论 在内毒素所致肝损伤中，NO起保护性作用，而ET-1则起促进作用，二者在肝脏中的作用可能是通过作用于肝筛而引起的。     

内皮素—1在内毒素灌注大鼠原位肝脏中的作用

应用肝脏原位灌注模型，探讨了内皮素１（ＥＴ１）在内毒素所致肝损伤中的作用。选用Ｗｉｓｔａｒ大鼠２４只，分为对照组、ＥＴ１组、内毒素组、内毒素＋ＥＴ１抗体组。观察了肝组织中ＥＴ１、一氧化氮（ＮＯ）、前列环素（ＰＧＩ２）、乳酸脱氢酶（ＬＤＨ）、丙二醛（ＭＤＡ）、三磷酸腺苷（ＡＴＰ）和肝组织学变化。结果显示：内毒素能使肝组织ＥＴ１含量增加；内毒素和ＥＴ１均能使细胞脂质过氧化物形成和酶的漏出，还能使肝细胞浊肿变性；ＥＴ１抗体能部分拮抗内毒素所致的肝损伤。结果表明：ＥＴ１参与了内毒素所致的肝损伤作用。     

Portal triad occlusion induces endotoxin tolerance: role of portal congestion

BACKGROUND: Portal triad occlusion (PTO) causes portal congestion and damages the intestinal mucosa, which is associated with portal endotoxemia. However, administration of a sublethal dose of endotoxin results in resistance to its toxic activities. We tested the hypothesis that portal congestion due to PTO induces endotoxin tolerance. MATERIALS AND METHODS: Rats were subjected to PTO for 15 min. In Group 1, male rats underwent laparotomy and, 48 h after the surgery, a lethal dose of Escherichia coli lipopolysaccharide was administered. In Group 2, rats were subjected to PTO for 15 min. Then a lethal dose of LPS was administered 48 h after surgery. Group 3 was treated the same as Group 2, except that PTO was performed with portosystemic shunt. Group 4 was also treated same as Group 2, except that rats received polymixin B and neomycin by gavage to eliminate intestinal luminal bacteria before PTO. Survival was examined after the administration of a lethal dose of LPS. Changes in plasma levels of cytokine are also measured after the administration of LPS. The portal endotoxin level in each group after PTO was measured. RESULTS: On survival test, only rats in Group 2 and Group 4 showed significantly higher survival rates. The portal endotoxin level was significantly elevated only in Group 2. The elevation of plasma cytokine levels (IL-6, TNF-alpha) and NO production (NO(2)(-)/NO(3)(-)) in Groups 2 and 4 were inhibited compare to those in Groups 1 and 3. CONCLUSIONS: PTO induced LPS tolerance possibly due to portal congestion and subsequent visceral congestion.     

Optimal portal venous circulation for liver graft function after living-donor liver transplantation

BACKGROUND: Previous studies have shown poor outcome after living-donor liver transplantation (LDLT) as a result of excessive portal venous pressure (PVP), excessive portal venous flow (PVF), or inadequate PVF. We investigated optimal portal venous circulation for liver graft function after LDLT in adult recipients retrospectively. METHODS: Between June 2003 and November 2004, 28 adult patients underwent LDLT in our institution. We modulated PVP under 20 mmHg in these 28 cases by performing a splenectomy (n=4) or splenorenal shunt (n=1). The PVF and PVP were measured at the end of the operation. Compliance was calculated by dividing PVF by PVP. RESULTS: PVF and compliance showed a significant inverse correlation with peak billirubin levels after LDLT (r = -0.63: r=-0.60, P<0.01), and with peak international normalized ratio after LDLT (r=-0.41: r=-0.51, P<0.05). Compliance was higher in right-lobe graft with middle hepatic vein cases (148+/-27 ml/min/mmHg), and lower in left-lobe graft cases (119+/-50 ml/min/mmHg). CONCLUSIONS: Liver graft function was better when PVF and graft compliance were higher and PVP was maintained under 20 mmHg.     

Improvement of morphological changes after 70% hepatectomy with portocaval shunt: preclinical study in porcine model

BACKGROUND: After extensive hepatectomy, excessive portal venous flow (PVF) and elevated portal venous pressure (PVP) may lead to postoperative liver damage. We have evaluated the use of portocaval shunt (PCS) to control PVF and PVP following partial hepatectomy (PH) to reduce the postoperative liver damage. METHOD: Twenty-four pigs were divided into two Groups: Group C (n = 10) underwent 70% PH alone and Group S (n = 14) underwent 70% PH with PCS. The changes in PVF, PVP, serum liver function tests, and histology were evaluated. RESULTS: PVP and PVF per unit of remnant liver weight and serum total bilirubin levels in Group S were significantly lower than those in Group C postoperatively (P < 0.05). Histology showed that there were significant differences in hepatocyte ballooning, necrosis, and neutrophil aggregation between the two groups (P < 0.05). In particular, hepatic necrosis was observed in zone 3 of Group C as centrilobular necrosis. These results suggest that hepatic and sinusoidal damage after 70% PH were more severe in Group C than in Group S, with the latter group maintaining an almost normal ultrastructural appearance. Hepatocyte apoptotic index differed significantly between the two groups (P < 0.0001). CONCLUSION: After 70% PH, extensive centrolobular necrosis and neutrophil aggregation were present and may have caused liver damage, manifested as hyperbilirubinemia and coagulopathy. The delayed liver regeneration with PCS may reduce the postoperative liver damages rather than the rapid liver hypertrophy. The diversion of PVF with PCS to maintain adequate PVP is a very effective procedure for avoiding the postoperative liver failure after extensive hepatectomy.