温阳解毒化瘀方对肝衰竭大鼠内毒素血症的影响

目的:动态观察温阳解毒化瘀方对肝衰竭大鼠内毒素血症(ITEM)的影响。方法:将85只SD大鼠随机分为正常组、模型组、对照组(予乳果糖+三联活菌溶液)及温阳解毒化瘀颗粒组(实验组),采用D-半乳糖胺(D-gal)腹腔注射致肝衰竭ITEM大鼠模型。正常组在腹腔注射生理盐水12小时后处死,其余各组分别于造模后12小时、24小时各取10只大鼠处死,检测各组大鼠血清转氨酶(ALT、AST)、肝组织病理学、门静脉及结肠内毒素水平。结果:模型组12小时时ALT和AST较正常组升高(P<0.05),24小时时门静脉及结肠内毒素水平明显升高(P<0.01),肝组织大面积坏死;实验组及对照组在造模后12小时各观察指标与模型组比较,差异无显著性意义,造模后24小时两组ALT和AST、门静脉及结肠内毒素水平较模型组降低(P<0.05),肝组织病变减轻。结论:D-gal腹腔注射可建立大鼠肝衰竭ITEM模型,温阳解毒化瘀方可通过降低门静脉及结肠内毒素水平减轻ITEM而达到抗肝衰竭的效应。     

逆灌注对移植肝缺血再灌注损伤的影响

目的:探讨原位肝移植中经下腔静脉逆行灌注对移植肝缺血再灌注损伤的影响.方法:36例大鼠肝移植随机分为3组,每组12例.门静脉组即经门静脉顺行灌注,肝动脉+门静脉组即同时开放肝动脉及门静脉顺行灌注,下腔静脉组即先吻合下腔静脉后开放逆行灌注,然后吻合门静脉及肝动脉.分别检测术后1、6及24 h的血清转氨酶、移植肝病理变化及...     

Effects of tumor necrosis factor, endothelin and nitric oxide on hyperdynamic circulation of rats with acute and chronic portal hypertension

AIM:To evaluate the effect of tumor necrosis factor (TNF),endothelin (ET) and nitric oxide (NO) on hyperdynamic circulation (HC) of rats with acute and chronic portal hypertension (PHT).METHODS: Chronic portal hypertension was induced in Wistar rats by injection of carbon tetrachloride. After two weeks of cirrhosis formation, L-NMMA (25mg/kg) was injected into one group of cirrhotic rats via femoral vein and the experiment was begun immediately. Another group of cirrhotic rats was injected with anti-rat TNFα (300mg/kg) via abdominal cavity twice within 48h and the experiment was performed 24h after the second injection. The blood concentrations of TNFα, ET-1 and NO in portal vein and the nitric oxide synthase (NOS) activity in hepatic tissue were determined pre-and post-injection of anti-rat TNFα or LNMMA. Stroke volume (SV), cardiac output (CO), portal pressure (PP), superior mesenteric artery blood flow (SMA flow) and lilac artery blood flow (IAflow) were measured simultaneously. Acute portal hypertension was established in Wistar rats by partial portal-vein ligation (PVL). The parameters mentioned above were determined at 0.5h,24h, 48h, 72h and 120h after PVL. After the formation of stable PHT, the PVL rats were injected with anti-rat TNFα or L-NMMA according to different groups, the parameters mentioned above were also determined.RESULTS:In cirrhotic rats, the blood levels of TNFα, NO in portal vein and the liver NOS activity were significantly increased (P&lt;0.05) while the blood level of ET-1 was not statistically different (P&gt;0.05) from the control animals(477.67&#177;83.81pg/mL vs 48.87&#177;32.79pg/mL, 278.41&#177;20.11μmol/L vs 113.28&#177;14.51μmol/L, 1.81&#177;0.06μ/mg.prot vs 0.87&#177;0.03μ/mg.prot and 14.33&#177;4.42pg/mL vs8.72&#177;0.79pg/mL, respectively). After injection of anti-rat TNFα,the blood level of TNFα was lower than that in controls (15.17&#177;18.79pg/mL vs 48.87&#177;32.79pg/mL). The blood level of NO and the liver NOS activity were significantly decreased, but still higher than those of the controls. The blood level of ET-1 was not significantly changed. PP,SV,CO, SMAflow and IAflow were ameliorated. After injection of L-NMMA, the blood level of NO and the liver NOS activity were recovered to those of the controls. PP and CO were also recovered to those of the controls. SV, SMAflow and IAflow were ameliorated. In PVL rats, the blood levels of TNFα NO in portal vein and the liver NOS activity were gradually increased and reached the highest levels at 48h after PVL. The blood level of ET-1 among different staged animals was not significantly different from the control animals. PP among different staged animals (2.4&#177;0.18kPa at 0.5h, 1.56&#177;0.08kPa at 24h, 1.74&#177;0.1kPa at 48h,2.38&#177;0.05 kPa at 72h, 2.39&#177;0.16 kPa at 120h) was significantly higher than that in controls (0.9&#177;0.16kPa). After injection of anti-rat TNFα in 72h PVL rats, the blood level of TNFα was lower than that in controls (14&#177;14pg/mL vs 48.87&#177;32.79pg/mL). The blood level of NO and the liver NOS activity were significantly decreased, but still higher than those of the controls. The blood level of ET-1 was not significantly changed. PP was decreased from 2.38&#177;0.05kPa to 1.68&#177;0.12kPa, but significantly higher than that in controls. SV, CO, SMAflow and IAflow were ameliorated.After injection of L-NMMA in 72h PVL rats, the blood level of NO and the liver NOS activity were recovered to those of the controls. PP, SV, CO, SMAflow and IAflow were also recovered to those of the controls.CONCLUSION:NO plays a critical role in the development and maintenance of HC in acute PHT and is a key factor for maintenance of HC in chronic PHT. TNFα may not participate in the hemodynamic changes of HC directly, while play an indirect role by inducing the production of NO through activating NOS. No evidence that circulating ET-1 plays a role in both models of portal hypertension has been found.     

胆管结扎肝硬变犬肝脏血管铸型研究

目的研究胆管结扎肝硬变犬肝脏血管形态变化，以探讨肝硬变时肝脏血液循环障碍的类型、程度和意义．方法将正常犬（ｎ＝６）和肝硬变犬（ｎ＝１０）的肝脏取出并处理后，用三种颜色铸型剂分别注入三种血管系统制作出肝血管铸型标本．结果肝硬变犬肝血管铸型主要表现：①门脉主干显著扩张，分支突然中断变细，呈残根状；各级分支形态畸变、走行失常，形成大量吻合支．②肝静脉分支畸变，或被血栓阻塞，或形成吻合支甚至血管瘤．③肝动脉充盈稀少，部分区域呈丛状增生．④肝内广泛门体分流．结论犬胆管结扎肝硬变时，肝内存在严重血管改建、血栓形成和血液循环紊乱．     

Role of hepatic artery in haemodynamics in normal and cirrhotic livers in rats

To examine the degree of influence of the hepatic artery on microcirculation in the liver, microscopic observation of blood flow in the hepatic minute blood vessels and the sinusoids and pressure measurements at key points in hepatic vascular pathways in vivo were performed before and after hepatic artery ligation in normal and cirrhotic rats. In normal rats, portal vein pressure (109 mmH2O) fell 10 mmH2O after hepatic artery ligation, but the pressures of the terminal portal venule, the terminal hepatic venule and the inferior vena cava did not change. In cirrhotic rats, portal vein pressure (206 mmH2O) and terminal portal venule pressure (106 mmH2O) fell 23 and 10 mmH2O after hepatic artery ligation respectively: the pressures in the terminal hepatic venule and the inferior vena cava did not change. These results suggests that the pressure transmitted from the hepatic artery was mostly supplied to the intrahepatic portal vein in normal rats and both to the intrahepatic portal vein and to the sinusoids in cirrhotic rats. In both normal and cirrhotic rats, however, the pressure transmitted from the hepatic artery was about 10 per cent of the initial portal vein pressure, and the blood flow in minute vessels and sinusoids did not change after hepatic artery ligation. Accordingly, it is believed that the hepatic artery plays only a small role in the haemodynamics of the liver in both normal and cirrhotic rats, irrespective of the distribution and manner of the hepatic arterial termination.     

Hepatic arterial flow becomes the primary supply of sinusoids following partial portal vein ligation in rats

BACKGROUND AND AIM: Partial portal vein ligation (PPVL) is a commonly used procedure to induce prehepatic portal hypertension in animal models. The aim of this study was to test the hypothesis that the hepatic arterial flow becomes the primary source feeding the sinusoids in the liver after PPVL. METHODS: Sprague-Dawley rats underwent either sham operation or partial portal vein ligation (PPVL). The number of vessels in the liver at 2 weeks postoperatively was determined by factor VIII immunolocalization and the gene expression of angiogenic factors was assessed by RT-PCR. The total hepatic arterial supply to the liver was measured using the fluorescent microsphere injection technique. To further test the hypothesis, two additional groups of rats underwent hepatic artery ligation (HAL) or PPVL plus HAL (PPHAL). The integrity of hepatic microcirculation was then evaluated in all four groups by intravital microscopy. RESULTS: At 2 weeks after operation, the number of vessels detected by factor VIII staining was significantly higher in PPVL compared to sham. Densitometric analysis of RT-PCR bands revealed a significant increase of vascular endothelial growth factor gene expression in PPVL compared to sham. Arterial flow to the liver measured by fluorescent microspheres was increased by 190% in PPVL compared to sham. When all four groups were compared, no prominent histological abnormality was observed in sham, HAL, and PPVL groups; however, PPHAL livers showed focal necrosis and inflammatory cell infiltration around the portal triads. Additionally, only the PPHAL livers showed a decreased sinusoidal diameter and significantly lower perfusion index (PPHAL 42.9+/-6.1; sham 85.7+/-7.0, PPVL 80.2+/-6.5, HAL 70.9+/-4.5). CONCLUSIONS: These results suggest that the hepatic artery flow becomes the primary source for the blood supply of sinusoids and the compensatory change in the hepatic arterial system plays a critical role in maintaining microcirculatory perfusion following the restriction of the portal vein flow by PPVL.     

乳果糖对肝癌切除术后血浆内毒素血症及肝损伤的防护作用

目的：探讨乳果糖对肝脏缺血再灌注后内毒素血症所致肝损伤的防护作用。方法：40例肝癌患者随机分为乳果糖组及对照组。测定两组肝癌手术患者肝门阻断前后门静脉血、外周静脉血内毒素以及术前、术后第1、3、7天肝功能检测结果,做统计学分析。结果：肝门阻断前,乳果糖组患者内毒素水平要低于对照组（t=27．60,P〈0．01）：肝门阻断后,两组患者内毒素水平均升高,但对照组更高,差异有极显著意义（t=12．72,P〈0．01）,说明乳果糖可以明显减轻内毒素血症。术前两组患者血中丙氨酸转氨酶（ALT）和天门冬氨酸转氨酶（AST）均高于正常参考值,但乳果糖组较对照组略低,差异有统计学意义（t=4．28,P〈0．01;t’=4．91,P〈0．05）,术后第3天两组患者ALT和AST升高的水平最高,两组问差异有统计学意义（t’=2．11,P〈0．05）。结论：肝切除术前患者口服乳果糖,能降低其肝缺血后血中内毒素水平,减轻肝脏的缺血再灌注损伤,改善肝脏功能,有利于术后肝功能的恢复,对于预防术后急性肝功能衰竭起一定作用。     

大白兔肝缺血再灌注损伤时血浆内毒素的变化及对肝肾功能的影响

目的探讨肝缺血再灌注损伤过程中,肠源性内毒素的动态变化和继发性肝肾功能损害。方法取27只健康成年新西兰大白兔,体重1.4~2.3?,随机分为对照组7只,另外20只作为实验组。以缺血10min(I10min)、缺血20min(I20min)、缺血30min(I30min)和分别再灌注30min(R30min)随机分为3组。对照组取门、腔静脉血测肝肾功能及血浆内毒素,实验组阻断第一肝门造成不同的缺血时段,松开血管夹再灌注30min,其余实验同对照组。结果实验组中血浆谷草转氨酶、谷丙转氨酶、尿素氮、肌苷含量及内毒素浓度均有升高,在I10min/R30min组即有升高,但与对照组相比差异无显著性(P>0.05);而后随着缺血时间的延长这些指标继续明显升高,至I30min/R30min组达最高值,与对照组比差异有显著性(P<0.05~0.01)。肾组织电镜观察发现I10min/R30min组肾脏超微结构无明显改变,而I20min/R30min组和I30min/R30min组肾脏超微结构损害明显。结论肝门阻断后门静脉系统淤血,致肠源性内毒素产生和移位;肝门再开放造成肝缺血再灌注损伤,且随着缺血时间的延长,门、腔静脉血中内毒素水平进行性升高,肝功能进一步损害,最终引起肝肾综合征。     

Partial portal arterialization in complete en bloc resection of the hepatoduodenal ligament and left lobe of the liver for hepatic hilar cancer

The complete resection of the hepatoduodenal ligament is associated with enormous surgical invasion, which frequently results in postoperative hepatic dysfunction secondary to interruption of the reconstructed artery. We administered partial portal arterialization by anastomosis of the gastroduodenal artery to the portal vein without reconstruction of the hepatic artery in the complete resection of the hepatoduodenal ligament with resection of the left lobe of the liver in a patient with hilar bile duct carcinoma. After division of the proper hepatic artery, the gastroduodenal artery was anastomosed in an end-to-side fashion to the trunk of the portal vein. After division of the portal vein, to prevent ischemia, a single catheter bypass was inserted into a branch of the mesenteric vein and the another side of the catheter was attached to the hepatic end, of the portal vein. The portal vein was reconstructed with the superficial femoral vein graft. The blood supply to the remaining liver was interrupted for only 15 min during which the proximal end of the superficial femoral graft was anastomosed to the hepatic end of the portal vein. Postoperative liver function has been stabilized and his postoperative course is uneventful without portal hypertension. One month postoperatively, angiography through the vessels nourishing the raised jejunum visualized intrahepatic arteries.     

Tempol 对肝硬化大鼠肝门阻断后肠道菌群移位及内毒素血症的作用

目的：探讨4-羟基-2,2,6,6-四甲基哌啶（Tempol）对肝硬化大鼠肝门阻断后肠道细菌移位和内毒素血症的作用。方法选择SD大鼠30只,采用四氯化碳诱导行肝硬化建模,将建模大鼠随机均分为假手术组（不阻断肝门）、对照组（阻断肝门）、实验组（阻断肝门前后静注Tempol ）。3组均取门静脉、腔静脉血检测血清内毒素,取肠系膜淋巴结、肝组织、肺组织行细菌培养,以及小肠黏膜形态与细胞凋亡检测。结果与假手术组及对照组比较,实验组可明显减少肝门阻断后的肠道细菌移位及血清内毒素水平（ P均＜0．05）。结论 Tempo1可有效地预防肝硬化大鼠肝门阻断后的肠道细菌移位和内毒素血症。     

Establishment of a new pig model for auxiliary partial orthotopic liver transplantation

AIM: To establish a new pig model for auxiliary partial orthotopic liver transplantation (APOLT). METHODS: The liver of the donor was removed from its body. The left lobe of the liver was resected in vivo and the right lobe was used as a graft. After the left lateral lobe of the recipient was resected, end-to-side anastomoses of suprahepatic inferior vena cava and portal vein were performed between the donor and recipient livers, respectively. End-to-end anastomoses were made between hepatic artery of graft and splenic artery of the host. Outside drainage was placed in donor common bile duct. RESULTS: Models of APOLT were established in 5 pigs with a success rate of 80%. Color ultrasound examination showed an increase of blood flow of graft on 5th d compared to the first day after operation. When animals were killed on the 5th d after operation, thrombosis of hepatic vein (HV) and portal vein (PV) were not found. Histopathological examination of liver samples revealed evidence of damage with mild steatosis and sporadic necrotic hepatocytes and focal hepatic lobules structure disorganized in graft. Infiltration of inflammatory cells was mild in portal or central vein area. Hematologic laboratory values and blood chemical findings revealed that compared with group A (before transplantation), mean arterial pressure (MAP), central venous pressure (CVP), buffer base (BB), standard bicarbonate (SB) and K+ in group B (after portal vein was clamped) decreased (P<0.01). After reperfusion of the graft, MAP, CVP and K+ restored gradually. CONCLUSION: Significant decrease of congestion in portal vein and shortened blocking time were obtained because of the application of in vitro veno-venous bypass during complete vascular clamping. This new procedure, with such advantages as simple vessel processing, quality anastomosis, less postoperative hemorrhage and higher success rate, effectively prevents ischemia reperfusion injury of the host liver and deserves to be spread.     

Source of blood supply and embolization treatment in cavernous hemangioma and sclerosis of the liver

AIM: To investigate the source of the blood supply in carvenous hemangioma of liver (CHL), and provide a feasible treatment for CHL via thehepatic artery.METHODS: (1) Portovenography, hepatic arteriography and portal vein staining were performed in 5 patients to determine the origin of the blood supply. Two casts of hepatic blood vessels from resected specimens were observed. (2) Clinical data from 75 patients (30 males, 45 females, aged 25-57 years, mean of 37.4) were obtained. Of these, 56 were of solitary type (44 on the right lobe, 12 on the left, with 4 having intraparenchyma), and 19 were of multiple type (9 on the right, 2 the left, 8 whole liver). Twenty-two patients were treated with sclerosis, 50 by embolization via hepatic artery, and 3 were excised.RESULTS: In the 5 cases where portography was used, the contrast medium did not enter the tumor, and the tumor appeared as low density area, with the intrahepatic branches of the portal vein pushed aside. In the 5 cases with where portal vein staining was used, the normal liver parenchyma stained a deep blue; however, the tumor was not stained. The tumor area appeared as a round vacant cavity in the 2 specimen casts. For the 72 patients treated with sclerosis or embolization via hepatic artery or through interventional method, the tumors diminished by 10%-30% in diameter, and no tumors grew larger.CONCLUSION: The blood supply of CHL originates from the hepatic artery. Tumors treated with sclerosis and embolization decreased in size or got fibrotic.     

Endotoxin-induced liver necrosis and intravascular coagulation in rats enhanced by portacaval collateral circulation.

The effects of intravenously administered endotoxin on the hepatic and systemic circulation as well as on the coagulation system were evaluated in normal rats (n = 26), in rats with experimental portal hypertension (n = 15), and in rats with portacaval anastomosis (n = 22). Endotoxin (1-5 mg/kg) in the normal rat leads to a prompt increase of transaminase activity and to a hyperdynamic circulation with a consequent increase in the total hepatic blood flow. In a later phase (6 h postoperatively) the hepatic artery dilated with a consequent hepatic arterial hyperperfusion. The coagulation system was affected with signs of consumption coagulopathy. In the rats with portal hypertension and portacaval collaterals as well as in those with portacaval anastomosis, the endotoxin injection resulted in acute liver necrosis within 12 to 15 hours. The hepatic artery became overdilated with a cardiac output fraction of 25% (normal 5-5%). Blood extravasates and thrombi, rich in fibrin, were detected in the liver. It is suggested that this exaggeration of the endotoxin effect was due to an impaired clearance function of the reticuloendothelial system, probably as consequence of portacaval collateral circulation. It is concluded that endotoxins (1) damage the liver even in a normal organism; (2) are potent to induce acute liver necrosis, if the reticuloendothelial system is altered; (3) have to be taken into consideration as contribution to the pathogenesis of acute as well as chronic liver diseases.     

Evidence against a role for endotoxin in the hyperdynamic circulation of rats with prehepatic portal hypertension

BACKGROUND/AIMS: Excessive formation of nitric oxide may mediate the generalized vasorelaxation and hyporesponsiveness to vasoconstrictors observed in portal hypertensive states. Endotoxin, released from the bowel and detoxified by the liver, could stimulate inducible nitric oxide synthase directly or indirectly via the cytokine cascade. This study investigated the effect of chronic intraperitoneal injection of polymyxin B, a neutralizing antagonist of endotoxin, on the hemodynamics of partially portal vein-ligated (PVL) rats. METHODS: Concomitantly with endotoxin (600 EU) and dactinomycin (80 microg), polymyxin B (0.1 mg) or normal saline (N/S) was administered via an intraperitoneal route to male Sprague-Dawley rats. Twenty-four hours later, mean arterial pressure was determined. In PVL rats polymyxin B (0.1 mg in 5 cc N/S) or N/S was given intraperitoneally twice daily from 2 days prior to operation until 5 days (short-term) or 14 days (long-term) after the operation. Long-term polymyxin B- or N/S-treated sham-operated rats were included as controls. Hemodynamic studies with a thermodilution technique were performed at the end of treatment. Blood samples were collected from another series of PVL rats with long-term treatment to determine plasma levels of endotoxin and tumor necrosis factor-alpha. Plasma levels of endotoxin and tumor necrosis factor-alpha were measured by Limulus assay and the ELISA method, respectively. RESULTS: With the dosage of 0.1 mg polymyxin B, hypotension in rats subjected to endotoxin and dactinomycin administration could be corrected (polymyxin B vs. placebo: 130.0+/-7.7 vs. 108.8+/-6.7 mm Hg, p<0.05). However, long-term or short-term treatment with the same dosage of polymyxin B failed to ameliorate the hyperdynamic circulation of PVL rats. In addition, long-term treatment with polymyxin B did not change systemic and portal hemodynamics in sham-operated rats. Plasma levels of endotoxin and tumor necrosis factor-alpha were comparable in PVL rats treated with long-term polymyxin B or N/S (p>0.05). CONCLUSIONS: Our findings do not support the role of endotoxin in the hyperdynamic circulation of PVL rats.     

软肝冲剂对肝炎肝硬化门脉高压患者血清一氧化氮、内皮素的影响

目的：观察软肝冲剂对肝炎肝硬化门脉高压患者门静脉主干内径及血流量、血流速度和血清一氧化氮（NO），内皮素（ET）的影响。方法：选择肝炎肝硬化门脉高压患者97例，随机分为两组，治疗组口服软肝冲剂，对照级以西药常规治疗，观察治疗后的总有效率、肝功能，门静脉主干内径及血流量、血流速度和血清NO、ET的变化。结果：经治疗后治疗组总有效率优于对照组（P＜0．05），患者ANT，TBil明显降低，Alb和A／G均明显升高，门静脉内径变窄，血流量增多，血流速度变快，同时NO及ET亦显著降低，与对照组比较，差异有显著性意义（P＜0．05或0．01）。结论：软肝冲剂治疗肝炎肝硬化门脉高压疗效显著，能明显改善肝功能，降低门静脉压力，其作用机制之一是降低血清NO、ET水平。     

The effects of arterialisation of the portal stump on liver function and hepatic haemodynamics in cirrhotic rats with a portacaval shunt

Liver blood flow (xenon-133 clearance method) and wedged hepatic venous pressure were studied in cirrhotic rats immediately after and 3 weeks following portacaval shunting (PCS), PCS and arterialisation of the portal stump with the left gastric artery (PCS-ART) or sham operation. Liver weight and function were compared 3 weeks after operation. Liver blood flow and wedged hepatic venous pressure were significantly reduced immediately after and 3 weeks following PCS. PCS-ART maintained liver blood flow and wedged hepatic venous pressure within the pre-operative range and prevented the liver atrophy and deterioration in liver function observed in rats with PCS. The results suggest that arterialisation of the portal vein with an artery which does not significantly increase sinusoidal pressure may be of benefit in preventing the early undersirable sequelae of PCS in man.     

Influence of splanchnic vascular infusion on the content of endotoxins in plasma and the translocation of intestinal bacteria in rats with acute hemorrhage necrosis pancreatitis

The main reason for the death of the patient with acute hemorrhage necrosis pancreatitis (AHNP) is pancreatic infection and multi-organ failure caused by endotoxemia and intestinal bacterial translocation[1-7]. However, the pathogenesis of endotoxemia and intestinal bacterial translocation remains a question[8-10]; moreover, no effective method of prevention and cure for it has been found till now[11 -15] In the present study, we infused low dose dopamine and low molecular weight dextran through the catheters to abdominal aorta and portal vein, and observed its influence on the endotoxin concentration in plasma and the rate of translocation of intestinal bacteria in AHNP rats.     

Regional and general effects of hepatic lobes with impaired blood flow after hepatic resection

BACKGROUND/AIMS: In hepatic surgery, blood flow to some parts of the liver may become impaired. At present, no consensus has been reached on ways to treat such affected parts of the liver with impaired blood supply. METHODOLOGY: After the ligation of branches of rat's hepatic artery and/or portal vein, the ligated and non-ligated lobes were studied at fixed intervals up to 84 days. Parameters include hepatic tissue blood flow assessed by a laser Doppler flowmeter, liver regeneration ability using bromodeoxyuridine, apoptosis using anti-single-stranded DNA Ig-G antibody, and vulnerability to an endotoxic injection. RESULTS: Hepatic artery ligation group showed no obvious changes in either the ligated or non-ligated lobes, and these lobes had no effects on the whole body. Of the portal vein ligation group, although the ligated lobes underwent marked atrophy, the compensatory hypertrophy of the non-ligated lobes took place sufficiently and no life-threatening conditions were observed. With regard to the hepatic artery/portal vein ligation (HA/PVL) group, hepatic blood flow in the ligated lobes rapidly decreased, and all hepatocytes underwent necrosis 1 day after surgery. In the non-ligated lobes, however, significant increases in the bromodeoxyuridine labeling index were detected at 1, 2, and 3 days after surgery, and compensatory hypertrophy was recognized. Indocyanine green 15-minute retention rate rapidly increased 1 day after surgery, and there were significant differences compared to the sham group up to 7 days after surgery. The postsurgical mortality rate in the HA/PVL group was significantly high at 13%, and mortality rate following endotoxin injection was as high as 75%. CONCLUSIONS: Affected parts of the liver with blockage of both the hepatic artery and portal vein should be resected.