肝硬变门静脉高压症患者肝脏体积测定及其临床意义

目的通过测定肝脏体积术前判断肝硬变门静脉高压症患者手术耐受能力和术后远期效果。方法使用双螺旋ＣＴ应用三维表面遮盖显示法检测了２５例肝硬变门静脉高压症患者的肝脏体积,并与对照组３０例比较。结果对照组肝脏大小与身高呈正线性相关,ｒ＝０４２（Ｐ＜００５）,平均肝体积为（１０７０６８±２２７５２）ｃｍ３,与肝硬变组（７９７０２±１３５１１）ｃｍ３比较差异有显著性意义（Ｐ＜００５）。肝硬变门静脉高压症患者肝体积与Ｃｈｉｌｄ分级有关,ＣｈｉｌｄＣ级患者肝脏明显小于ＣｈｉｌｄＢ级患者（６７２４±９１１）ｃｍ３,（８８８２±９２６）ｃｍ３,Ｐ＜００５。结论肝体积小者分流术后易发生脑病,但肝脏大小、门静脉血流量和门体自然分流率没有密切的相关关系。     

非肝病患者肝组织结构上H1和H2受体的放射自显影研究

目的 探讨正常人肝组织结构上Ｈ１和Ｈ２受体的分布。方法 用光学放射自显影术对８名非肝病患者肝组织进行定位研究。结果 Ｈ１，Ｈ２受体广泛分布于肝细胞和肝内血管壁上，以Ｈ２受体占优势，肝细胞上的Ｈ１，Ｈ２受体显著高于各血管壁（Ｐ〈０．０５），Ｈ２受体肝静脉壁上最高，显著高于肝动脉和门静脉（Ｐ〈０．０１）。结论 肝细胞上的缚胺受体可能参与了组胺的代谢，组胺对肝血流动力学的影响可能是以肝静脉壁上Ｈ２受体介     

氨甲酰血红蛋白在评价血液透析充分性中的意义

目的　评价氨甲酰血红蛋白（ Ｃａｒ Ｈｂ） 在血液透析（ Ｈ Ｄ） 充分性中的意义。方法　用高效液相色谱法测定正常对照组３６ 例,非透析慢性肾功能衰竭５１ 例和 Ｈ Ｄ 患者３０ 例 Ｃａｒ Ｈｂ 含量（ 以每克血红蛋白含氨甲酰缬氨酸微克数,μｇ Ｃ Ｖ／ｇ Ｈｂ 表示） 。 Ｈ Ｄ 组 Ｃａｒ Ｈｂ 含量与尿素清除指数（ Ｋｔ／ Ｖ） 、尿素降低率（ Ｕ Ｒ Ｒ） 、平均时间尿素浓度（ Ｔ Ａ Ｃｕｒｅａ） 和校正蛋白质分解率（ｎ Ｐ Ｃ Ｒ） 作相关分析。结果　与对照组（３００ ±６１） 比较, Ｈ Ｄ 组 Ｃａｒ Ｈｂ 含量（１０２５ ±２８９） 显著升高（ Ｐ＜ ００１） ,但显著低于非透析组（１３９９ ±５２０）（ Ｐ＜ ００１） ; Ｋｔ／ Ｖ≤１１ 组 Ｃａｒ Ｈｂ 显著高于 Ｋｔ／ Ｖ＞ １１ 组［（１３５０ ±３１０）ｖｓ．（８８６±１２０） , Ｐ＜ ００１］ ; Ｃａｒ Ｈｂ 与 Ｋｔ／ Ｖ, Ｕ Ｒ Ｒ 呈负相关,但与 Ｔ Ａ Ｃｕｒｅａ 正相关。当 Ｋｔ／ Ｖ＞ １１ ,ｎ Ｐ Ｃ Ｒ＜ １０ ｇ· Ｋｇ１·ｄ１ 组 Ｃａｒ Ｈｂ 显著高于ｎ Ｐ Ｃ Ｒ≥１０ ｇ· Ｋｇ１·ｄ１ 组［（９６５ ±８３）ｖｓ．（８１５ ±１０４） , Ｐ     

小剂量重组人红细胞生成素在尿毒症患者的药物动力学和药效学观察

目的观察小剂量重组人红细胞生成素治疗尿毒症贫血的药物动力学和疗效及对血压的影响，探索更为有效、安全的用药方案。方法红细胞生成素测定采用酶联法。起始剂量２０Ｕ／ｋｇ每日静脉注射，维持Ｈｃｔ３０％～３５％。结果５例尿毒症未透析患者静脉和皮下注射２０Ｕ·ｋｇ－１／ｄ后，１／２消除速率常数（ｋｅ）分别为１４３±７０和７０±３１小时（Ｐ＜００１），平均驻留时间（ＭＲＴ）分别为２０３±４８和８０±２４小时（Ｐ＜００１）；皮下注射后生物利用度（Ｆ）为２３６％±８２％。４７例尿毒症患者治疗２周后Ｈｃｔ显著升高，贫血纠正期总剂量仅为常规剂量（１００Ｕ／ｋｇ每周３次）皮下及静脉组的５５％～６０％和７１％～７１３％（Ｐ＜００１），血压升高发病率显著低于常规剂量组（８５％和２０９％，Ｐ＜００５）。结论本药小剂量每日静脉注射能显著提高对贫血的疗效，降低高血压发生率。     

断流术对门静脉高压症患者肝脏血流动力学及肝功能的影响

目的观察断流术对门静脉高压症肝血流动力学改变及肝功能的影响。方法应用超声多普勒分别检测２５例门静脉高压症患者手术前后门静脉血流量（ＰＶＦ）、肝动脉血流量（ＨＡＦ），采用水柱法测量自由门静脉压力（ＦＰＰ）的变化，应用吲哚氰绿１５分钟潴留率（Ｒ１５ＩＣＧ）分别估测患者手术前后的肝功能。结果ＰＶＦ由术前的（１３２３±３８８）ｍｌ／ｍｉｎ减少至术后的（８９５±２６２）ｍｌ／ｍｉｎ（Ｐ＜００１）；ＨＡＦ由术前的（３７０±７０）ｍｌ／ｍｉｎ增加至术后的（４８５±１２３）ｍｌ／ｍｉｎ（Ｐ＜００１）；ＦＰＰ由术前的（２８±４）ｍｍＨｇ降至术后的（２５±４）ｍｍＨｇ（Ｐ＜００５）；Ｒ１５ＩＣＧ由术前的（１９±７）％变至术后的（２１±７）％（Ｐ＞００５）。结论断流术后门静脉血流量虽然减少，但是肝动脉血流量增加及术后门体分流的减少均利于术后硬变肝脏的功能维护。     

经颈内静脉肝内门体分流术对门静脉高压症患者门静脉及全身血流动力学影响

目的研究经颈内静脉肝内门体分流术（ＴＩＰＳＳ）对门静脉和全身血流动力学的影响。方法采用超声多普勒、直接门静脉测压和血气分析、ＳｗａｎＧａｎｚ导管对１５例门静脉高压症患者检测ＴＩＰＳＳ术前后门静脉、体循环和肺循环血流动力学的变化。结果ＴＩＰＳＳ术后３０分钟和２周，门静脉压力下降３４％和５５４％，氧分压和氧饱和度增加６７７％、２１３％和６８０％、２０４％。术后２周门静脉血流速度增加１４倍，心输出量显著增加（Ｐ＜００１），外周血管阻力和肺血管阻力显著下降（Ｐ＜００１），右心房压和肺动脉压增加（Ｐ＜００５）；肾血流量显著增加（Ｐ＜００１），肾功能明显改善。结论ＴＩＰＳＳ既有效降低门静脉压力和改善肾脏功能，又加重门静脉和全身血流高动力状态，应用时需加强心、肝功能的监护     

门静脉高压症患者血儿茶酚胺浓度及其拮抗剂的作用

为了解儿茶酚胺类递质在肝硬变门静脉高压症发病中的作用，作者测定了１３例经病理证实的坏死后肝硬变门静脉高压症患者及３４例无肝脏和心血管疾病的对照者周围静脉血中的肾上腺素及去甲肾上腺素的浓度，并观察了从周围静脉输入α肾上腺素受体拮抗剂酚妥拉明前后肝硬变门静脉高压症患者肝静脉楔入压、自由肝静脉压和肝静脉压力梯度的变化。结果显示肝硬变组周围血肾上腺素和去甲肾上腺素浓度分别为５３．４±２３．９ｐｇ／ｍｌ，４４６．０±３１０．７ｐｇ／ｍｌ，显著高于对照组２３．５±１１．２ｐｇ／ｍｌ，１８３±８３．３ｐｇ／ｍｌ，（Ｐ＜０．０１）。持续静点酚妥拉明后肝静脉楔入压及肝静脉压力梯度显著下降（肝静脉楔入压下降０．５５～０．６３ｋＰａ，Ｐ＜０．０１；肝静脉压力梯度下降０．６２ｋＰａ，Ｐ＜０．０１）。本研究结果表明：肝硬变门静脉高压患者存在着明显的儿茶酚胺类递质代谢紊乱，其对内脏血流动力学的影响与门静脉高压症的发生、发展有密切关系；α－肾上腺素受体拮抗剂酚妥拉明能有效地降低门静脉压力。     

大块肝切除后急性肝损伤治疗的研究

将６０只大鼠随机分为２组，一组腹腔内注射肝细胞生长因子（ＨＧＦ）和１，６二磷酸果糖（ＦＤＰ），另一组代之以生理盐水做为对照，分别于术后３、７、１４天检测血清酶学变化、胃泌素含量和体外肝细胞培养蛋白质合成及ＤＮＡ合成。结果发现：治疗组大鼠术后３天ＡＬＴ较对照组迅速降低（Ｐ＜０．０１）；血浆脯肽酶（ＰＬＤ）在术后７天、１４天低于对照组（Ｐ＜０．０５）；血清胃泌素测定在术后３天、７天治疗组高于对照组（Ｐ＜０．０１）；肝细胞体外原代培养￣３Ｈ－亮氨酸掺入法显示治疗组术后３天蛋白质合成明显高于对照组（Ｐ＜０．０１）；￣３Ｈ－ＴｄＲ掺入肝细胞ＤＮＡ合成，治疗组术后各期均非常显著高于对照组（Ｐ＜０．０１）。结果证实大鼠大块肝切除后应用ＨＧＦ和ＦＤＰ，对急性肝损伤有重要的治疗作用。     

肝硬变门静脉高压症患者血肾上腺素,去甲肾上腺素浓度测定

作者使用高效液相色谱检测了肝硬变门静脉高压症患者（３８例）、原发性高血压患者（２４例）和对照病人（３４例）周围静脉血及上腔静脉、周围动脉、门静脉血肾上腺素和去甲肾上腺素浓度。肝硬变组及原发性高血压组患者周围血肾上腺素浓度分别为５７．５±３７．４ｐｇ／ｍｌ和５４．９±３９．９ｐｇ／ｍｌ，差异无显著意义，但与对照组（２３．５±１１．２ｐｇ／ｍｌ）相比浓度均有显著升高（Ｐ＜０．０１）。肝硬变组及原发性高血压组患者周围血去甲肾上腺素浓度分别为４５１．１±３８１．２ｐｇ／ｍｌ和５２４．３±２１ｐｇ／ｍｌ，与对照组相比（１８３．０±８３．３ｐｇ／ｍｌ）差异有极显著意义（Ｐ＜０．０１）。术中取上腔静脉、动脉和门静脉血分别比较肾上腺素和去甲肾上腺素浓度，除上腔静脉血肾上腺素浓度的差异有显著意义外（８３．７±４６．７ｐｇ／ｍｌ与２０７．２±５５．４ｐｇ／ｍｌ，Ｐ＜０．０５），其余差异均无显著意义。本研究结果表明肝硬变门静脉高压症患者存在着明显的儿茶酚胺类递质的代谢紊乱，其对患者全身及内脏血流动力学的影响与门静脉高压症发生发展的关系值得深入研究。     

人肝癌裸鼠转移模型中纤溶酶原激活物抑制剂变化与肝癌生物学特性

目的研究纤溶酶原激活物抑制剂（ＰＡＩ１）与肝细胞癌（ＨＣＣ）生物学特性的关系。方法构建ＬＣＩＤ２０人肝细胞癌裸鼠转移模型（肝癌转移模型）４０例,用ＰＡＩ１试剂盒和ＰＡＩ１单抗分别做酶活性检测和免疫组化,观测肝癌转移模型发展过程中ＰＡＩ１的变化。结果肝癌转移模型从肿瘤发生早期（２周）至晚期（５周）,血浆ＰＡＩ１从６２±１８Ａｕ／ｍｌ增至１５４±０７Ａｕ／ｍｌ,Ｐ＜００５。肿瘤组织中ＰＡＩ１从０４±０１Ａｕ／ｍｇ增至０８±０３Ａｕ／ｍｇ;血浆中ＰＡＩ１改变与肿瘤大小和ＡＦＰ变化相关（ｒ＝０９６４８和ｒ＝０９５４４,Ｐ＜００５和Ｐ＜００５）。结论肝癌转移模型肿瘤组织及血浆中ＰＡＩ１随ＨＣＣ病程进展逐步升高。ＰＡＩ１与ＨＣＣ肿瘤增长和ＡＦＰ升高有良好的相关性。ＰＡＩ１与ＨＣＣ侵袭性及预后密切相关     

肝硬化门静脉高压症患者肝脏组织α1紧上腺素受体亚型的mRNA表达

目的 探讨肝硬化门静脉高压症患者肝脏组织α１肾上腺素受体亚型ｍＲＮＡ的表达。方法 应用半定量逆转录聚合酶链反应检测了１２例乙型肝炎后肝硬化门静脉高压症患者和１５例无高血压,无肝脏疾患的胆石症或胃肠道肿瘤患者肝脏组织α１肾上腺素受体亚型ｍＲＮＡ的表达。在同一体系中同时逆转录并扩增α１肾上腺素受体亚型特异性片段和内参ＧＡＰＤＨ片段,以二者的积分密度比值作为该受体亚型的ｍＲＮＡ相对表达量。结果 肝脏组织     

生长抑素对肝硬变门静脉高压症患者门静脉,肝静脉血流和门静？…

目的 了解生长抑素对肝硬变门静脉高压症患门静脉、肝表脉血液动力学及门静脉压力的影响。方法 用彩色多普勒超声系统测定了２０例肝硬变门静脉高压症患使用生长抑素前后门静脉主干及左、中、右３支肝静脉的内径、最大血流速度及其血流量。其中１５例患测定生长抑素前后门静脉压力的变化。结果 １５例患使用生长抑素后１、１．５小时,门静脉压力由用药前的２．７７±０．２６ｋＰａ下降至２．４２±０．２７ｋＰａ和２．     

肝硬变患者门腔静脉分流术前后胰高血糖素水平的动态观察

目的 研究肝硬变门静脉高压症患者行门腔静脉分流术后血浆胰高血糖素水平的变化。方法 应用放射免疫分析法测定了１６例肝硬变门静脉高压闰行门腔静脉分流术和１６例对照组患者血浆Ｇｌｃ水平。     

Splanchnic cortisol production in dogs occurs primarily in the liver: evidence for substantial hepatic specific 11beta hydroxysteroid dehydrogenase type 1 activity

Eight dogs underwent combined hepatic/portal vein catheterization and infusion of D4-cortisol in order to determine the relative contributions of the viscera and liver to splanchnic cortisol production. D4-cortisol concentrations progressively decreased from 2.6 +/- 0.1 to 2.4 +/- 0.1 to 1.7 +/- 0.1 microg/dl (P < 0.001 by ANOVA) from hepatic artery to portal vein to hepatic vein, respectively, indicating 8 +/- 3 and 28 +/- 3% extraction across the viscera and liver, respectively. On the other hand, hepatic artery, portal vein, and hepatic vein cortisol concentrations did not differ (0.31 +/- 0.12 vs. 0.28 +/- 0.11 vs. 0.27 +/- 0.10 microg/dl, respectively), indicating zero net cortisol balance. This meant that 1.0 +/- 0.1 microg/min of cortisol was produced within the splanchnic bed, all of which occurred within the liver (1.2 +/- 0.1 microg/min). On the other hand, visceral cortisol production did not differ from zero (-0.2 +/- 0.2 microg/min; P < 0.001 vs. liver). Flux through the 11beta hydroxysteroid dehydrogenase (HSD) type 1 pathway can be measured by determining the rate of conversion of D4-cortisol to D3-cortisol. D3-cortisol concentrations were lower in the portal vein than hepatic artery (0.45 +/- 0.03 vs. 0.48 +/- 0.02, respectively; P < 0.01) but did not differ in the portal vein and hepatic vein, indicating net uptake across the viscera but zero balance across the liver. D3-cortisol production with the viscera and liver averaged 0.2 +/- 0.1 microg/min (P = NS vs. zero production) and 0.6 +/- 0.1 microg/min (P < 0.001 vs. zero production; P < 0.001 vs. viscera production), respectively. We conclude that most, if not all, of splanchnic cortisol production occurs within the liver. Taken together, these data suggest that the high local cortisol concentrations generated via the 11beta HSD type 1 pathway within the liver likely contribute to the regulation of hepatic glucose, fat, and protein metabolism.     

Study on splanchnic circulation: measurement of the liver blood flow

In anesthetized patients during abdominal surgery, hepatic artery and portal vein flows were measured simultaneously utilizing an ultrasonic transit-time volume flowmeter. The total hepatic blood flow was 994.6 +/- 52.4 ml/min. The hepatic artery flow and the portal vein flow were 260.0 +/- 23.8 ml/min and 730.8 +/- 41.3 ml/min, respectively. The ratio of hepatic artery flow to portal vein flow was 0.37 +/- 0.04. A significant increase in hepatic artery flow (p less than 0.01) followed portal vein occlusion, whereas no significant change was observed in portal vein flow after hepatic artery occlusion. Common hepatic artery occlusion resulted in a significant decrease in hepatic artery flow (p less than 0.05), but no significant change was observed in portal vein flow. The present study firstly demonstrated that ultrasonic transit-time volume flowmeter is a device to quantitatively assess hepatic artery and portal vein flows with good reproducibility and stability in human subjects. This easy and simple technique seemed to have wide clinical application to abdominal surgery and would have a promising in studying splanchnic blood flows in various situations such as in cases of hepatectomy and portal hypertension.     

肝硬变腹水患者门腔静脉分流术后肾素活性,血管紧张素转换酶？…

目的 探讨肝硬变腹水患者行门腔静脉分流术前后肾素活性（ＰＲＡ）、血管紧张素转换酶（ＡＣＥ）、血管紧张素Ⅱ水平及门静脉压力（ＰＶＰ）的变化。方法 应用光度比色 放射免疫分析法,对１６例肝硬变合并腹水的患者行门腔静脉分流术前后和１６例行胃肠道肿瘤切除手术的且患者,手前后的门静脉、外周静脉和动脉血中的ＰＲＡ、ＡＣＥ、ＡⅡ及ＰＶＰ进行了测定。结果 肝硬变组门腔静脉分流前后的ＰＢＡ、ＡＣＥ、ＡⅡ及ＰＶＰ显著     

肝硬变时肝内门静脉系统血管顺应性的研究

目的用隔离灌流的鼠肝硬变模型（ＩＰＣＭ）观测肝内血管的顺应性。方法８０只四氯化碳（ＣＣｌ４）诱导肝硬变大鼠,按门静脉单纯灌流和门静脉肝动脉联合灌流分为Ａ、Ｂ两组,通过递增灌流速度观察模型血流动力学变化。结果Ａ组中,对照组基础压力为１６５±０２８ｋＰａ,与此相比,每分钟灌流速分别为３５ｍｌ,４５ｍｌ,５５ｍｌ的３个实验组灌注压随着灌流速度的梯度增加而迅速升高,二者间有高度相关性（ｒ＝０９８５,Ｐ＜００１）,肝内阻力变化不大（Ｐ＞００５）;每分钟灌流速为１５ｍｌ的Ｑ１５组则由于低灌流造成了模型的不可逆损伤。ＩＰＣＭ最大灌流速度范围小于文献报告的正常肝脏灌流的相应范围。Ｂ组中,Ｑ３５～Ｑ５５组的灌注压力也呈迅速升高趋势（Ｐ＜００５）,但未发生Ｑ１５组的低灌流现象;与Ａ组相比,Ｂ组由于开放了肝动脉灌流而部分地缓解了门静脉的压力升高。结论（１）肝硬变门静脉高压症时肝内循环顺应性下降而向肝血流量增加;（２）肝动脉与门静脉两系统间可能存在血流动力学功能的相互代偿     

Portal hyperperfusion causes disturbance of microcirculation and increased rate of hepatocellular apoptosis: investigations in heterotopic rat liver transplantation with portal vein arterialization

Clinical results of portal vein arterialization (PVA) in liver transplantation are controversial. One reason for this is the lack of a standardized flow regulation. Our experiments in rats compared PVA with blood-flow regulation to PVA with hyperperfusion in heterotopic auxiliary liver transplantation (HALT). In group I (n = 19), the graft's portal vein was completely arterialized via the right renal artery in-stent technique, using a 0.3-mm stent, leading to a physiological average portal blood flow. In group II (n = 19), a 0.5-mm stent was used. In group II, the average portal blood flow after reperfusion was significantly elevated (group II: 6.4 +/- 1.5; group I: 1.7 +/- 0.4 mL/min/g of liver weight; P < .001). The sinusoidal diameter after reperfusion was significantly greater in group II (9.8 +/- 0.5 microm) than in group I (5.5 +/- 0.2 microm; P < .001). Red blood cell velocity in the dilated sinusoids was significantly lower in group II (171 +/- 18 microm/s) than in group I (252 +/- 13 microm/s). Stasis of erythrocytes occurred; consequently, the functional sinusoidal density was significantly reduced in group II (38 +/- 7%) compared with group I (50 +/- 3%; P < .01). Two hours after reperfusion of the portal vein, the number of apoptotic hepatocytes was significantly higher in group II than in group I (I: 0 +/- 0 vs II: 7 +/- 9 M30-positive hepatocytes/10 high-power fields). The 6-week survival rate was 9 of 11 in both groups. In group II, 6 of 9 grafts showed massive hepatocellular necroses after 6 weeks, whereas in group I, only 1 of 9 presented a slight hepatocellular necrosis. Finally, our results demonstrate negative effects of portal hyperperfusion in transplanted livers, which are correctable by adequate flow regulation.     

Effect of dopamine infusion (3-30 microg/kg/min) on hepatic hemodynamics

BACKGROUND: While dopamine produces well-characterized dose-dependent effects on systemic hemodynamics, there is a paucity of information regarding its effects on hepatic hemodynamics. Infusion rates above 10 microg/kg/min are reported to produce significant vasoconstriction and impair organ perfusion. Therefore, donors are sometimes considered unsuitable when higher doses of dopamine are in use. The aim of this study was to determine the effect of increasing doses of dopamine on hepatic hemodynamics in a nonanesthetized swine model. MATERIALS AND METHODS: Sixteen pigs were instrumented with indwelling catheters in a peripheral artery, peripheral vein, portal vein, and hepatic vein and flow probes around the portal vein and hepatic artery. After recovery, the following variables were measured 10 +/- 1 days postinstrumentation: hepatic arterial flow (HAF), portal venous flow (PVF), mean systemic arterial pressure (MAP), central venous pressure (CVP), portal venous pressure (PVP), hepatic venous pressure (HVP), heart rate (HR). Recordings were obtained at baseline and subsequently when dopamine was infused at rates of 3, 6, 12, 15, 21, and 30 microg/kg/min increasing at 1-h intervals. RESULTS: HAF and PVF increased linearly over the entire infusion range, to 69 and 13% over baseline, respectively (P < 0.001, P < 0.05). Total hepatic blood flow rose 23% over baseline at the 30 microg/kg/min dosage (P < 0.01). MAP increased linearly 13% over the range 12 to 30 microg/kg/min (P < 0.001). CVP, HVP, and PVP did not change significantly. HR decreased from 12 to 15 microg/kg/min (P < 0.01), then increased from 15 to 30 microg/kg/min (P < 0.05). CONCLUSION: These data show that dopamine infused at dosages of 3-30 microg/kg/min augments HAF, PVF, and THBF and that this effect is linear. These results suggest high-dose dopamine infusion does not disqualify a potential donor liver for transplantation.     

Intraoperative estimation of liver blood flow in man.

The intraoperative measurement of the afferent circulation of the liver, namely the hepatic artery flow and portal venous flow was carried out upon 14 anaesthetized patients having carcinoma of the splanchnic area, mainly in the head of the pancreas, by means of transit time ultrasonic volume flowmeter. The hepatic artery flow, portal venous flow and total hepatic flow were 0.377 +/- 0.10; 0.614 +/- 0.21; 0.992 +/- 0.276 l/min, respectively. The ratio of hepatic arterial flow to portal venous flow was 0.66 +/- 0.259. There was a sharp, significant increase in hepatic arterial flow (29.8 +/- 6.1%, p < 0.01) after the temporary occlusion of portal vein, while the temporary occlusion of hepatic artery did not have any significant effect on portal venous circulation. The interaction between hepatic arterial flow and portal venous flow is a much disputed question, but according to the presented data here, it is unquestionable, that the decrease of portal venous flow immediately results a significant increase in hepatic artery circulation.