快速补流对门静脉血液动力学的影响

探讨急性失血性休克，对肝硬门静脉高压犬门静脉系统血流动力学，和快速补液对门静脉压力等指标恢复的影响。方法肝硬化门脉高压犬模型造成急性ＨＳ，并于ＨＳ后给予快速补液抗休克，插管直接测定门静脉压力、平均动力脉压、肝脏血流量。结论：肝硬化ＨＳ后，快速补液后ＰＶＰ会早于ＭＡＰ迅速升高并超过休克前水平，ＰＶＰ达到正常水平时所需补液明显小于失血量。     

丹参对门脉高压血流动力学影响的实验与临床研究

为研究丹参对肝硬化门脉血流动力学的影响，利用血管插管测定用药前后胆管结扎肝硬化犬门脉系统压力变化，超声多普勒监测肝硬化患者用药后门静脉系统血流动力的改变。结果：（１）丹参静脉给药可使肝硬化犬门静脉压（ＰＰＶ）、嵌塞肝静脉压（ＷＨＶＰ）、肝静脉压力梯度（ＨＶＰＧ）显著降低（Ｐ＜０．０５～０．０１），而平均动脉压（ＭＡＰ）、心率（ＨＲ）无明显变化（Ｐ＞０．０５）；（２）丹参长期口服（１０～１２周），可显著降低肝硬化患者（Ｃｈｉｌｄ－ＰｕｇｈＡ、Ｂ级）门静脉内径（ＤＰＶ）、脾静脉内径（ＤＳＶ）、门静脉血流量（ＱＰＶ）、脾静脉血流量（ＱＳＶ）（Ｐ＜０．０５～０．０１），并对患者乏力、厌食、腹胀及肝功能（ＡＬＴ）具有部分改善作用，未见副作用。本研究表明，丹参为安全有效的降低门静脉压力药物，值得对其做进一步研究。     

门静脉高压患者门静脉压力与血流动力学的相关性研究

目的 探讨门静脉高压患者门静脉血流动力学的变化特点及其与门静脉压力的相互关系。方法 采用彩色多普勒超声对４１例肝硬化门静脉高压患者（Ｃｈｉｌｄ Ａ、Ｂ级３１例、Ｃ级１０例）于手术前检测门静脉（ＰＶ）、脾静脉（ＳＶ）和肠系膜上静脉（ＳＭＶ）的内径和血流速度，再计算出相关的面积和血流量；于手术时对３１例ＣｈｉｌｄＡ十Ｂ级患者直接测量门静脉压力。３２例健康人和２６例慢性乙型肝炎患者（慢肝组）作为对照。结累 门静脉高压两组患者ＰＶ、ＳＶ和ＳＭＶ内径（ｃｍ）分别为１．５１和１．５２、１．３２和１．３４及１．１５和１．１５较慢肝组和正常组明显增宽，ｒ分别为１．３１和１．１６、０．９６和０．７９及０．９１和０．８２（Ｐ＜０．０１）；血流速度较正常组和慢肝组明显减慢（Ｐ＜０．０１）；门静脉高压Ｃ级组门静脉血流速度（ｃｍ／ｓ）为４．６５较门静脉高压Ａ十Ｂ级组（６．４２）明显减慢（Ｐ＜０．０１），而两组 ＳＶ和 ＳＭＶ的血流速度则差异无显著意义（Ｐ＞０．０５）；门静脉高压 Ａ＋Ｂ级组三条静脉的血流量明显大于正常组和慢肝组（Ｐ＜０．０１或Ｐ＜０．０５）；门静脉高压Ｃ级组门静脉血流量明显小于Ａ十Ｂ级组（Ｐ＜０．０１）；而ＳＶ和ＳＭＶ的血流     

当归对肝硬化门脉高压影响的临床与实验研究

目的和方法：通过对胆管结扎肝硬化犬门脉系压力的直接测定，超声多普勒监测肝硬化患者的门脉血流，研究当归对肝硬化门脉血流动力学的影响。结果：（１）当归静脉给药，肝硬化犬的门静脉压（Ｐｐｖ）、嵌塞肝静脉压（ＷＨＶＰ）、肝静脉压力梯度（ＨＶＰＧ）显著降低（Ｐ＜００５～００１），平均动脉压（ＭＡＰ）、心率（ＨＲ）无明显变化（Ｐ＞００５）；（２）当归口服用药后（１０～１２周），肝硬化患者门静脉内径（Ｄｐｖ）、脾静脉内径（Ｄｓｖ）、脾静脉血流量（Ｑｓｖ）显著降低（Ｐ＜００５～００１），门静脉血流量（Ｑｐｖ）降低无显著意义（Ｐ＞００５）。结论：用药后，患者症状与肝功能（ＡＬＴ）部分好转，未见副作用。表明，当归为降低门静脉高压安全有效的药物     

肝硬化大鼠内脏血管组织内皮素及其基因表达的研究

目的探讨肝硬化大鼠内脏血管组织中,内皮素（ＥＴ）及其基因表达量的变化在门静脉高压形成机制中的意义。方法用放射免疫法分别测定大鼠血浆以及门静脉（ＰＶ）和肠系膜上动脉（ＳＭＡ）组织中ＥＴ含量,采用ＲＴ－ＰＣＲ技术分析ＰＶ和ＳＭＡ组织中ＥＴｍＲＮＡ表达量的变化。结果ＰＶ和ＳＭＡ组织中ＥＴ及其ｍＲＮＡ表达量,肝硬化组均显著高于正常对照组（均为Ｐ＜０．００１）;而肝硬化大鼠血管组织ＥＴ含量及ＥＴｍＲＮＡ表达量,则为ＰＶ明显高于ＳＭＡ（＜０．０５）,但正常对照组动静脉之间差异无显著性（Ｐ＞００５）。另外,内脏动静脉血管ＥＴ含量之差与门静脉压力呈显著的正相关。结论ＥＴ可能通过更多的收缩内脏静脉特别是门静脉,增加门静脉血流阻力而参与门静脉高压的形成。     

当归对正常及肝硬化犬门脉血液动力学的影响

研究当归对正常（ｎ＝６）和慢性胆管结扎肝硬化犬（ｎ＝８）的全身和门脉血液动力学的影响。结果表明，给正常及肝硬化犬静滴当归注射液（８０ｍｇ／ｋｇ／ｍｉｎ），可以明显降低正常犬ＭＡＰ（１９．４５：１７．３４ｋＰａ，Ｐ＜０．０２），对ＨＲ和ＩＶＣＰ没有影响，但肝硬化犬ＭＡＰ、ＨＲ和ＩＶＣＰ均没有明显变化。相反，应用当归注射液后肝硬化犬ＷＨＶＰ（２．４２±０．８０：１．７９±０．７６ｋＰａ，Ｐ＜００１）、ＨＶＰＧ（１．６９±０．７０：１．０６±０．６８ｋＰａ，Ｐ＜００１）、Ｐｐｖ（２．５０±０．７９：１．８１±０．７４ｋＰａ，Ｐ＜０．００１）和Ｒｐｖ（０．８９±０．４８：０．５８±０．４０ｋＰａ·Ｓ／Ｌ，Ｐ＜００１）显著下降，但Ｑｐｖ、ＱＨＡ和ＱＴＬ治疗前后基本保持稳定。研究证明，当归注射液是一种治疗门脉高压的安全有效药物。     

丹参与肝硬变犬门脉压力及胃粘膜血流的影响

通过胆总管结扎法，制造犬肝硬变门高压模型，并直接测定丹参注射液对肝硬变犬门脉压力及胃粘膜轿流（ＧＭＢＦ）的影响。结果表明，静注丹参注射液后，肝硬变犬的门脉压力（Ｐｐｖ）嵌塞肝静脉压（ＷＨＶＰ）、肝静脉压力梯度（ＨＶＰＧ）显著下降（Ｐ〈０．０１），平均动坟（ＭＡＰ）、心率（ＨＲ）无显著变化（Ｐ〉０．０５）。给药后１０ｍｉｎ，肝硬变及正常犬的ＧＭＢＦ显著增加（Ｐ〈０．０５），用药后３０ｍｉｎ达最高值（     

丹参等活血化淤中药对门脉高压血流动力学影响的临床与实验研究

目的探讨丹参、当归等及硝苯啶对门脉高压血流动力学的影响。方法采用血管插管测定胆管结扎肝硬化犬门脉系统压力变化；超声多普勒观测肝硬化患者门脉血流动力学变化。结果（１）静脉滴注丹参、当归后，肝硬化犬门静脉压（Ｐｐｖ）、嵌塞肝静脉压（ＷＨＶＰ）、肝静脉压力梯度（ＨＶＰＧ）显著降低（Ｐ＜０．０５～０．０１），平均动脉压（ＭＡＰ）、心率（ＨＲ）无明显变化（Ｐ＞０．０５），硝苯啶则使Ｐｐｖ，ＷＨＶＰ，ＭＡＰ．ＨＲ显著降低（Ｐ＜０．０５）。（２）丹参、丹参＋硝苯啶．丹参＋水＋硝苯啶口服药１０－１２周，能显著降低肝硬化患者门静脉内径（Ｄｐｖ）、脾静脉内径（Ｄｓｖ）．门静脉血流量（Ｑｐｖ），脾静脉血流量（Ｑｓｖ）（Ｐ＜０．０５－０．０１，当归作用较弱。结论对比表明，丹参、当归等中药较硝苯啶对门脉压力作用为慢，但较持久，无副反应。     

乳糖化清蛋白单磷酸阿糖腺苷的抗鸭乙型肝炎病毒作用

目的了解乳糖化清蛋白单磷酸阿糖腺苷（ＬＨＳＡＡｒａＡＭＰ）体内抗鸭乙型肝炎病毒（ＤＨＢＶ）的作用，为临床治疗乙肝患者提供实验基础．方法采用麻鸭乙型肝炎动物模型，用ＬＨＳＡＡｒａＡＭＰ２５ｍｇ／（ｋｇ·ｄ），１次／ｄ，治疗１０ｄ，观察用药前后（０，５，１０及１３ｄ）血清中ＤＨＢＶＤＮＡ，ＤＨＢｓＡｇ，肝脏组织病理学变化以及药物的毒副反应．结果ＬＨＳＡＡｒａＡＭＰ用药后能使血清ＤＨＢＶＤＮＡ水平显著降低，对血清ＤＨＢｓＡｇ作用相对较缓，治疗过程中未见ＬＨＳＡＡｒａＡＭＰ的毒副反应．结论该药既降低了单磷酸阿糖腺苷（ＡｒａＡＭＰ）的使用剂量，避免了ＡｒａＡＭＰ的副反应，又能抑制ＤＨＢＶ的复制，在体内达到抗ＤＨＢＶ的作用．     

肝硬化大鼠内脏血管壁NOS分布的免疫组化研究

目的：观察肝硬化门静脉高压大鼠内脏动、静脉血管壁一氧化氮合酶（ＮＯＳ）的分布及染色强度变化,探讨ＮＯ在门静脉高压形成机制中的作用。方法：采用免疫组化染色法,应用两种ＮＯＳ特异性抗体,分别观察内皮型（ｅＮＯＳ）和诱生型（ｉＮＯＳ）ＮＯＳ的变化特点,并结合计算机图象分析系统对染色强度进行量化处理。结果：肝硬化大鼠肠系膜上动脉（ＳＭＡ）ｉＮＯＳ和ｅＮＯＳ染色强度与对照组相比均显著增加（Ｐ＜０．０１）,其中以ｅＮＯＳ增加更为明显。而两组门静脉（ＰＶ）ＮＯＳ染色强度则无明显差异（Ｐ＞０．０５）。肝硬化组ＳＭＡ的ＮＯＳ染色强度明显高于ＰＶ（Ｐ＜０．０５）。结论：ＮＯＳ在内脏血管表达增多,以及在ＳＭＡ的表达高于ＰＶ,提示ＮＯ可能主要通过扩张内脏动脉、增加内脏血流量而参与门静脉高压的形成。     

不同静脉灌注量对门静脉高压失血性休克犬血流动力学的影响

目的 研究门静脉高压犬失血性休克时不同静脉灌注量对血流动力学的影响。方法 行缩窄门静脉主干1/2加丝线慢性栓塞术建立犬肝前性门静脉高压症模型,2周后股动脉快速放血制失血性休克模型,分大剂量、小剂量组静脉灌注复苏休克,观察不同静脉灌注量对门静脉高压失血性休克犬血流动力学的影响。结果 肝前性门静脉高压犬在失血性休克期血流动力学发生一系列改变,加重门静脉高压症时存在的血流动力学紊乱。快速静脉灌注复苏休克后,平均动脉压（MAP）、下腔静脉压（IVCP）、门静脉压（PVP）、门静脉压力梯度（PVPG）、门静脉血流量（PVBF）、肝动脉血流量（HABF）及肝血流量（HBF）均迅速上升,大剂量静脉灌注组升高幅度均较小剂量静脉灌注组大。PVR、SVR、HAR均显著降低。大剂量静脉灌注复苏休克,PVP、PVPG、PVBF、HABF、HBF出现反跳式升高,超过基线水平PVA达（3.28±0.34）kPa。而小剂量静脉灌注复苏休克时PVPG、PVP、PVBF、HABF、HBF与MAP、IVCP改变大致平行,无此反跳式升高,PVP至（2.34±0.26）kPa。大剂量静脉灌往组PVPG较PVP升高更早,更显著,并且超过基础值的 13％,达（2.58±0.37）kPa,故其发生再出血的危险性大为增加。小剂量静脉灌柱组PVPG一直低于基线水平,而且较基础值降低22％以上,至（1.67±0.27）     

Combination of preoperative embolization of the right portal vein and hepatic artery prior to major hepatectomy in high-risk patients: a preliminary report

BACKGROUND/AIMS: Preoperative transhepatic portal vein embolization may not always be sufficient to achieve the desired changes in contralateral hepatic volume and function. The beneficial role of additional transcatheter arterial embolization performed after inadequate response to preoperative transhepatic portal vein embolization is described. METHODOLOGY: Four patients underwent both preoperative transhepatic portal vein embolization and transcatheter arterial embolization, and 6 control patients underwent preoperative transhepatic portal vein embolization only. Changes in right liver lobe volume fraction, residual left lobe volume fraction, and prediction score (low-risk, < 45; borderline, 45-55; high-risk > 55); were evaluated. RESULTS: 1) The change in right liver lobe volume after both preoperative transhepatic portal vein embolization and transcatheter arterial embolization (volume after/before) was 0.75 times that of the original level whereas after preoperative transhepatic portal vein embolization, they were only 0.81 times that of the original level. 2) The change in residual left liver volume after both preoperative transhepatic portal vein embolization and transcatheter arterial embolization (volume after/before) was 1.40 times that of the original level whereas after preoperative transhepatic portal vein embolization they were only 1.30 times than the original level. The changes in left liver volume after preoperative transhepatic portal vein embolization/transcatheter arterial embolization was more favorable than those after preoperative transhepatic portal vein embolization only. 3) The change in prediction score after both preoperative transhepatic portal vein embolization and transcatheter arterial embolization (after/before) was 0.81 times that of the original level. All prediction score in high-risk patients recovered to the borderline or safety zone. Change after preoperative transhepatic portal vein embolization only (before/after) was 0.87 times that of the original level. 4) All 4 patients who underwent both preoperative transhepatic portal vein embolization and transcatheter arterial embolization received right hepatic lobectomy successfully and returned to their normal life style. CONCLUSIONS: Preoperative occlusion of right hepatic inflow vessels increased the volume and function of the contralateral lobe where high-risk patients recovered to the borderline zone for major hepatic resection.     

Hepatic hemodynamics and functions in extrahepatic portal obstruction in the rat with liver cirrhosis

Portal vein obstruction due to a thrombus may be encountered in liver cirrhosis. However, the effect of portal vein obstruction on hepatic hemodynamics and functions, and on collateral formation has not been clear in liver cirrhosis. To rectify this, the cirrhotic rat model with portal vein ligation was evaluated. In addition to the early recovery of hepatic blood flow, the reduction in hepatic blood flow after portal vein ligation was less in the cirrhotic rat than in the normal rat. The portogram showed that, in addition to hepato-fugal collaterals, hepato-petal collaterals developed well and early in the cirrhotic rat as compared with the normal rat. Although mitochondrial functions before portal vein ligation deteriorated in the cirrhotic rat, the decrease after portal vein ligation was less, and the recovery of function was earlier in the cirrhotic than the normal rat. The influence of portal vein obstruction on hepatic hemodynamics and functions in the cirrhotic rat was less than in the normal rat, due to earlier and significant formation of hepato-petal collaterals.     

Hepatic hemodynamics in 24 patients with nodular regenerative hyperplasia and symptomatic portal hypertension

Background and Aim: To evaluate hepatic hemodynamics in patients with nodular regenerative hyperplasia of the liver (NRH) with portal hypertension (PHT). Methods: We retrospectively reviewed the charts of 24 patients referred for PHT related to biopsy‐proven NRH. Hemodynamic measurements included wedged hepatic vein (WHVP) and inferior vena cava (IVCP), and, in 12 patients, portal vein pressure (PVP). Hepatic vein pressure gradient (HVPG: WHVP–IVCP) and portal vein pressure gradient (PVPG: PVP–IVCP) were calculated. Results: Nodular regenerative hyperplasia was associated in 24 patients with various diseases (oxaliplatin chemotherapy, treatment with purine antagonists, post liver transplantation, hematologic and rheumatologic conditions and HIV infection). Liver function parameters were either completely normal or slightly impaired. Patients were referred for gastroesophageal varices (n = 18), and/or ascites (n = 11), and/or splenomegaly (n = 20). In patients with varices or ascites, HVPG was lower than 10 mmHg (a cut‐off point for the presence of varices and/or ascites) in 15/21, suggesting a pre‐sinusoidal component to their PHT confirmed by a PVP higher than 12 mmHg in 12/12 patients. The mean difference between HVPG and PVPG was 8.7 mmHg in these patients. Ten patients were treated by transjugular intrahepatic portosystemic shunt. None of them re‐bled, and one presented transient hepatic encephalopathy. Conclusions: Presinusoidal PHT associated with NRH is probably related to compression of portal venules by the regenerative nodules. In patients with HTP and a HVPG < 10 mmHg, the diagnosis of NRH must be suspected and PVP measured, which is important in the management of these patients.     

Heat shock protein 70 induction in hepatocytes after right portal vein embolization

BACKGROUND/AIMS: Preoperative right portal vein embolization enhances remnant liver function following massive hepatectomy. Several studies have reported an increase in the volume of the left hepatic lobe after right portal vein embolization, but little information exists regarding heat shock protein induction in hepatocytes after right portal vein embolization. The objective of this study is to determine whether heat shock protein is induced in hepatocytes after right portal vein embolization in patients who underwent extended right hepatic lobectomy. METHODOLOGY: Four patients with gallbladder cancer and one patient with intrahepatic cholangiocellular carcinoma who underwent extended right hepatic lobectomy combined with caudate lobectomy and resection of the extrahepatic bile duct after right portal vein embolization were enrolled in this study. Operation was performed 21-36 days after right portal vein embolization. At operation, small liver specimens were taken immediately after laparotomy from both the right anterior segment (embolized lobe) and lower part of the left medial segment (non-embolized lobe) and heat shock protein 70 was induction in these specimens was measured by Western blotting. RESULTS: Heat shock protein 70 was induced in the left lobe relative to the right lobe in four patients, three of whom had an uneventful postoperative course. CONCLUSIONS: This paper is the first report to show the induction of heat shock protein 70 in the non-embolized hepatic lobe after right portal vein embolization in the clinical cases.     

双剂量奥曲肽对肝硬化门脉高压症断流术后患者血流动力学的影响

目的研究双剂量奥曲肽对肝硬化门脉高压症断流术后患者门脉压力、肝脏血流动力学影响。方法肝硬化门脉高压症断流术患者26例,随机分两组,术后24h开始用奥曲肽。A组12例,奥曲肽50μg／h;B组14例,奥曲肽25μg／h;胃网膜右静脉插管至门静脉主干,动态测定门脉压力;彩色超声多普勒测定门脉直径（PV）、门脉最大血流速度（PFVmax）、门脉平均血流速度（PFVmean）、肝动脉最大血流速度（HAVmax）、肝动脉最小血流速度（HAVmin）;计算门脉血流量参数（PFI）、肝动脉血流量参数（HAFI）。结果断流术后,两组患者门脉压力平均降幅15．4％,PFI降低（P〈0．05）;HAVmax、HAVmin、HAFI增加（P〈0．05）。用奥曲肽72h后,两组PFI、PFVmax、PFVmean降低（P〈0．05）;用药5min门脉压力降低,24h达高峰,门脉压力平均降幅20．6％。A组停药后48h内,门脉压力未见回升,平均降幅23．1％;B组停药后2h门脉压力有回升趋势,平均降幅11．6％;停药后24h、48h两组患者门脉压力比较差异有统计学意义（P〈0．01）。Logistic分析发现,PV、PFVmax、PFVmean、HAVmax、HAVmin与门脉压力无独立相关性。结论肝硬化门脉高压症患者行断流术后,门脉压力降低。双剂量奥曲肽均能明显降低门脉压力;停药后48h内,奥曲肽50μg／h组门脉压力未见回升。提示,临床用奥曲肽50μg/h对防止静脉曲张再出血更合理。     

Participation of the arterial and portal drainage in the calculation of total hepatic blood flow in guinea pigs

Experiments were performed on partly isolated livers of guinea pigs. The hepatic outflow (HOF) was measured by an electromagnetic flowmeter placed on the inferior vena cava. Nutritive hepatic blood flow (HBF) was measured with ¹³³Xe bolus technique with the tracer injected into the portal vein or hepatic artery. Under unchanged perfusion conditions, three exponents could be demonstrated irrespective of the site of injection. Two of them observed during the first 5 min represent the intrahepatic, the third (slowest one) the extrahepatic blood flow. Occlusion of either the portal vein or the hepatic artery results in a monoexponential decrease during the first 5 min. Calculation of the HBF was based on an equation including both components of the washout curves obtained after arterial and portal application. The calculated HBF was equal to the value of the directly measured total outflow but overestimated HBF_f calculated from the first exponent of the washout curve obtained after intraportal tracer application.     

Effects of posture change on the hemodynamics of the liver

BACKGROUND/AIMS: According to our experience, blood flow in the portal vein may alter according to body posture. It is reported that decreased portal venous flow immediately gives rise to significantly increased blood flow in the hepatic artery. To gain further insight into blood flow changes affected by posture, we examined blood flows in the portal vein, hepatic artery and hepatic vein at different postures. METHODOLOGY: Using a Doppler ultrasound system, the hemodynamics of the portal vein, right hepatic artery, and hepatic vein were examined in 35 patients at supine and left decubitus positions. RESULTS: Portal vein blood flow volumes were significantly lower in the left decubitus position than in the supine. In the right hepatic artery, the left decubitus position gave significantly higher blood flow velocity values than the supine. CONCLUSIONS: Our results indicated that upon change of posture from the supine to left decubitus position, portal vein flow velocity was reduced and hepatic artery flow velocity increased. Changes in portal and hepatic arterial flows by changing posture may be explained by decreased portal flow as a direct result of changed posture, leading to increased hepatic arterial flow to maintain total hepatic blood inflow.     

Regulatory processes interacting to maintain hepatic blood flow constancy: Vascular compliance, hepatic arterial buffer response, hepatorenal reflex, liver regeneration, escape from vasoconstriction

Constancy of hepatic blood flow (HBF) is crucial for several homeostatic roles. The present conceptual review focuses on interrelated mechanisms that act to maintain a constant HBF per liver mass. The liver cannot directly control portal blood flow (PF); therefore, these mechanisms largely operate to compensate for PF changes. A reduction in PF leads to reduced intrahepatic distending pressure, resulting in the highly compliant hepatic vasculature passively expelling up to 50% of its blood volume, thus adding to venous return, cardiac output and HBF. Also activated immediately upon reduction of PF are the hepatic arterial buffer response and an HBF-dependent hepatorenal reflex. Adenosine is secreted at a constant rate into the small fluid space of Mall which surrounds the terminal branches of the hepatic arterioles, portal venules and sensory nerves. The concentration of adenosine is regulated by washout into the portal venules. Reduced PFreduces the washout and the accumulated adenosine causes dilation of the hepatic artery, thus buffering the PF change. Adenosine also activates hepatic sensory nerves to cause reflex renal fluid retention, thus increasing circulating blood volume and maintaining cardiac output and PF. If these mechanisms are not able to maintain total HBF, the hemodynamic imbalance results in hepatocyte proliferation, or apoptosis, by a shear stress/nitric oxide-dependent mechanism, to adjust total liver mass to match the blood supply. These mechanisms are specific to this unique vascular bed and provide an excellent example of multiple integrative regulation of a major homeostatic organ.     

Portal venous arterialization resulting in increased portal inflow and portal vein wall thickness in rats

AIM： To explore the influence of portal vein hemodynamic changes after portal venous arterialization （PVA） on peribiliary vascular plexus （PVP） morphological structure and hepatic pathology, and to establish a theoretical basis for the clinical application of PVA. METHODS： Sprague-Dawley rats were randomly divided into control and PVA groups. After PVA, hemodynamic changes of the portal vein and morphological structure of hepatohilar PVP were observed using Doppler ultrasound, liver function tests, ink perfusion transparency management and three-dimensional reconstruction of computer microvisualization, and pathological examination was performed on tissue from the bile duct wall and the liver. RESULTS： After PVA, the cross-sectional area and blood flow of the portal vein were increased, and the increase became more significant over time, in a certain range. If the measure to limit the flow in PVA was not adopted, the high blood flow would lead to dilatation of intrahepatic portal vein and its branches, increase in collagen and fiber degeneration in tunica intima. Except glutamic pyruvic transaminase （GPT）, other liver function tests were normal. CONCLUSION： Blood with a certain flow and oxygen content is important for filling the PVP and meeting the oxygen requirement of the bile duct wall. After PVA, It is the anatomic basis to maintain normal morphology of hepatohilar bile duct wall that the blood with high oxygen content and high flow in arterialized portal vein may fill PVP by collateral vessel reflux. A adequate measure to limit blood flow is necessary in PVA.