Simultaneous sampling of portal, hepatic and systemic blood during intragastric loading and tracer infusion in conscious pigs

A surgical model for catheterization at multiple sites has been developed for use in long-term metabolic studies. For blood sampling, catheters were inserted into the portal and hepatic veins and the common carotid artery. The hepatic vein catheter was inserted from the margin of a liver lobe and led through the venous system, until the tip was close to the bifurcation with the inferior vena cava. A new technique was developed to ensure correct placement of the hepatic vein catheter using the specific extraction of indocyanin-green over the liver during surgery. Gastrostomy was performed using a Pezzer catheter. Catheters in the artery and hepatic and portal veins were patent for blood withdrawal for up to 4 weeks, and thus allowed repeated metabolic studies. Studies were performed in conscious animals familiar with the experimental situation.     

Distribution of the major histocompatibility complex antigens on different cellular components of human liver

Monoclonal mouse antibodies to the "framework" determinants of the class I and II molecules of the major histocompatibility complex (MHC) were used to demonstrate the presence of the MHC antigens in human liver. First, the localization of these antigens was demonstrated from frozen section histology with indirect FITC immunofluorescence and the cell component(s) binding the mouse antibody were identified by rabbit marker antisera and indirect TRITC immunofluorescence. Second, the antigen expression on the cell surface was analyzed by the Staphylococcus aureus rosette method from cytological cell smears. All antibodies reacted with cells in the liver sinusoids, both with the Kupffer cells and at least partially with the sinusoidal endothelial cells. The same antisera reacted also with the bile duct cells, though weaker, and with some stromal cells in close proximity of the blood vessels. The vascular endothelial cells of hepatic artery, hepatic vein, and portal vein displayed no reaction. Thus human liver differs strikingly from, e.g., human kidney, where the vascular endothelial cells contain large amounts of MHC antigens on the cell surface. This difference may be one explanation to why liver allografts are less promptly rejected than renal allografts in man.     

Transport of amino acids in the splanchnic bed by blood plasma and blood in the preruminant calf]

Three preruminant calves were fitted with catheters in portal and hepatic veins and in a mesenteric artery. Two electromagnetic flowmeter probes were clipped around the portal vein and the hepatic artery. The calves were fed either a diet with a low (L) or a high (R) abomasal emptying rate for dietary proteins. Blood flow and free amino acid levels in plasma (P) and blood (S) were determined before the morning meal and during the following 7 h. In the portal vein, for most amino acids P/S ratios were correlated to the net amino acid balance of the digestive tract measured in plasma. By contrast in the hepatic vein, these ratios were mainly correlated to hepatic balance measured in whole blood. Correlations between digestive tract and hepatic balance calculated using either plasma or whole blood pool were different for some amino acids. This suggests that amino acid exchange between plasma and blood cells is low and absorbed amino acids are mainly transported to the liver by plasma, whereas whole blood rather than plasma is concerned in amino acid exchanges in the liver.     

Preferential expression of connexin37 and connexin40 in the endothelium of the portal veins during mouse liver development

Hepatic blood vessels consist of the hepatic artery and three types of venous channels (the portal veins, the sinusoids, and the hepatic veins). This study was undertaken to analyze, by immunohistochemistry, connexin expression throughout the vascular development of the fetal mouse liver with special attention being given to portal vein development. In the adult liver, connexin37 and connexin40 were expressed in the endothelium of the portal vein and hepatic artery, but not in those of the hepatic vein and sinusoids. Connexin43 was expressed in mesothelial cells and smooth muscle cells of the portal veins. The preferential expression of connexin37 and connexin40 in portal veins was seen throughout liver development, including its primordium formation stage (10.5-day or 11.5-day stage), although connexin37 expression was transiently seen in free nonparenchymal cells in fetal stages. The differentiation of each blood vessel in the hepatic vascular system may occur in early developmental stages, soon after hepatic primordium formation. This work was supported by Special Coordination Funds for Promoting Science and Technology from the Ministry of Education, Culture, Sports, Science and Technology, Japan.     

Method for measuring hepatic uptake of oxygen or other blood-borne substances in situ.

A preparation is described by which hepatic arterial blood flow and portal venous blood flow can be accurately and continuously measured while simultaneously providing a method by which multiple blood samples can be taken from the hepatic artery, portal vein, and hepatic vein without disrupting hepatic hemodynamics or causing hemodilution. By this means hepatic uptake or release of blood-borne substances can be measured in situ and correlated with hemodynamic parameters. In 13 splenectomized cats, oxygen uptake by the denervated liver was 4.5 +/- 0.3 ml . min-1. 100 g-1 of tissue, representing 54% of total oxygen removed by the splanchnic bed. The hepatic hemodynamics determined by this method are similar to those reported by others in vivo and the metabolic state of the liver remained stable for at least 2 h during which an average of 29 blood samples were taken. Advantages of this preparation over other methods of obtaining similar data are discussed.     

Trichinella spiralis: vascular recirculation and organ retention of newborn larvae in rats

The recirculation of Trichinella spiralis newborn larvae was studied in inbred AO rats. Newborn larvae collected after in vitro incubation of adult T. spiralis worms for 2 or 24 hr were injected into rats through the tail vein or hepatic portal vein. Blood samples from the femoral vein, hepatic portal vein, and abdominal aorta were collected at intervals from 1 min to 24 hr after larval injection. Newborn larvae of both ages (24 hr or 2 hr old) persisted in femoral vein blood for less than or equal to 5 hr after injection, but they could be detected in portal vein blood by 24 hr after injection. The injection of larvae into a tail vein or the portal vein did not influence the pattern of larval circulation, although there was a 1-5 min delay in newborn larval appearance time after injection into the portal vein. Transcapillary migration through tissue and back to the circulation was evident in the appearance of newborn larvae in the thoracic duct lymph up to 24 (occasionally 48) hr after tail vein injection of newborn larvae. During the course of a natural primary infection, no evidence for trapping of larvae in the mesenteric lymph node could be found despite direct larval migration through this organ. Injected newborn larvae were retained in the lungs, and small numbers could be recovered 24 hr after intravenous injection. We conclude that a proportion of newborn larvae recirculates within the vasculature for several hours; a smaller population extravasates but can reenter the circulatory system via the lymphatics. Furthermore, some newborn larvae are found in organs rich in capillaries up to 24 hr after their entry into the blood.     

Local and metastatic growth of Lewis lung carcinoma as a function of its transplantation site. Application to the study of the pharmacology of sulphadiazine triazene]

The presence of a local tumour and pulmonary metastases is studied after the administration of the Lewis Lung Carcinoma at different sites of transplantation. The intravenous administration routes, in the tail vein and in the portal vein, injections in the liver and in the muscle of the left hindleg are used. The injection in the tail vein induces pulmonary "metastases". The injection in the portal vein is followed by multiple tumours in the whole liver and pulmonary metastases. An unilobar hepatic tumour and early pulmonary metastases appear after transplantation in the liver. Intra-muscular injection gives a local tumour which can be weighed after amputation of the leg and pulmonary metastases. A test of treatment by Sulphadiazine Triazene points out a weak action on the primary tumour and a larger one on the metastases.     

Evidence for a migratory capability of rat Kupffer cells to portal tracts and hepatic lymph nodes

The present study concerns the migratory ability of Kupffer cells in the rat. Phagocytic cells were labeled with colloidal carbon or gold, these markers being administered intravenously either into a tail vein, which resulted in generalized reticuloendothelial uptake, or in low dose into the portal vein, which produced uptake by Kupffer cells alone. Cells containing marker were observed in the portal tracts and in hepatic lymph nodes from 1 to 3 days after injection into the portal vein. The direct movement of single marker particles to the portal tracts could be excluded. Since injection of marker into the portal vein labeled Kupffer cells exclusively, whereas blood cells, splenic and bone marrow macrophages remained unlabeled, the labeled cells in the portal tracts and hepatic lymph nodes appeared to be former Kupffer cells migrating which had migrated to these sites.     

Vascular adhesion protein-1 mediates adhesion and transmigration of lymphocytes on human hepatic endothelial cells

Vascular adhesion protein-1 (VAP-1) is an amine oxidase and adhesion receptor that is expressed by endothelium in the human liver. The hepatic sinusoids are perfused by blood at low flow rates, and sinusoidal endothelium lacks selectin expression and has low levels of CD31, suggesting that VAP-1 may play a specific role in lymphocyte recruitment to the liver. In support of this we now report the constitutive expression of VAP-1 on human hepatic sinusoidal endothelial cells (HSEC) in vitro and demonstrate that VAP-1 supports adhesion and transmigration of lymphocytes across these cells under physiological shear stress. These are the first studies to report the function of VAP-1 on primary human endothelial cells. Under static conditions lymphocyte adhesion to unstimulated HSEC was dependent on VAP-1 and ICAM-2, whereas adhesion to TNF-alpha-stimulated HSEC was dependent on ICAM-1, VCAM-1, and VAP-1. Under conditions of flow, blocking VAP-1 reduced lymphocyte adhesion to TNF-alpha-treated HSEC by 50% and significantly reduced the proportion of adherent lymphocytes that transmigrated across cytokine or LPS-activated endothelium. In addition, inhibition of the amine oxidase activity of VAP-1 reduced both adhesion and transmigration of lymphocytes to a level similar to that seen with VAP-1 Ab. Thus, VAP-1 can support transendothelial migration as well as adhesion, and both functions are dependent on its enzymatic activity. In the absence of selectins and CD31, VAP-1 may play a specific role in lymphocyte recruitment via hepatic sinusoidal endothelium. Moreover, since VAP-1 is induced on nonhepatic endothelium in response to inflammation, its ability to support lymphocyte transendothelial migration may be an important systemic function of VAP-1.     

Influence of hepatic cells on allogeneic islet transplantation in rats without immunosuppressive drugs.

With the hypothesis of a possible helpful effect of the liver on islets transplanted into it, we have performed experiments that suggest some effect of hepatic cells for islet tolerance. We have studied 6 groups of Wistar rats made diabetic with streptozotocin and transplanted in sham conditions and with a mixture of islets and hepatic cells (allo-co-transplantation) in several conditions, all of them via the portal vein, and observed them over 30 days. Groups were as follows: Group A had a sham transplantation with saline. Group B was transplanted with hepatic cells alone. Group C was transplanted with islets alone without hepatic cells. Group D was co-transplanted with cultured islets and fresh hepatic cells (ratio 1:100). Group E was as group D with a ratio of 1:200. Group F also had co-transplantation, but after co-culture of islets and hepatic cells for 24 hours. Results show reversion of diabetes in group D for 4-5 days, and thereafter, a fall of blood glucose during the period observed. The effect was less marked in group F after co-culture of islets and hepatic cells. Paradoxically, when the ratio of islets and hepatic cell were 1:200, the results were not so good. These results suggest that hepatic cells have some helpful effect on islets when co-transplanted in the liver via the portal vein. More studies are needed to clarify if this effect can be related to some hepatic cell subpopulation; also if the effect is a membrane one, cell-to-cell contact, or through some secreted product.     

Combined Hepatic Vein, Umbilicoportal Vein, and Superior Mesenteric Artery Catheterization in Portal Hypertension: Estimation of the Portal Fraction of Total Hepatic Blood Flow in Cirrhotic Patients

Hemodynamic data were obtained in 13 cirrhotic patients with severe portal hypertension, undergoing combined hepatic vein, umbilicoportal vein, and superior mesenteric artery catheterization. The relative clearance of indocyanine green, the portohepatic gradient (difference between the free portal venous pressure and the free hepatic venous pressure), and the estimated hepatic blood flow were measured. The portal fraction (PF) of total hepatic blood flow was calculated in all patients using indicator dilution curves obtained from the portal bifurcation, a right hepatic vein, and when possible a left hepatic vein (six cases) after injection of ⁵¹Cr-labeled red blood cells (⁵¹Cr RBC) into the superior mesenteric artery. Flows were overestimated because of loss of indicator through spontaneous portosystemic shunts; however, the ratio between hepatic and portal indicator dilution curves can be used to calculate the portal fraction of total hepatic blood flow since no extrahepatic shunts existed after the bifurcation of the portal vein (as shown on portography). In 10 patients, 15 series of curves were calculable and the PF varied between 30.1 and 100% (mean ± SE: 71.1 ± 6.2%). In the three other patients, only delayed activity from recirculation was detected from portal and hepatic vein samples and PF was 0%; in these three cases, portography and arteriography revealed spontaneous portacaval shunting with reverse and/or stagnant circulation in the portal vein. In the 13 patients, no correlation existed between PF and the relative clearance of indocyanine green or the portohepatic gradient, parameters generally used as indices of severity in cirrhosis. In 10 patients, no correlation was found between PF and the estimated hepatic blood flow.     

The Role of miRNA-34a as a Prognostic Biomarker for Cirrhotic Patients with Portal Hypertension Receiving TIPS

Background

Circulating miRNA-34a is increased in blood of patients with different liver diseases when compared to healthy controls. However, the origin of miRNA-34a and its possible relationship with hemodynamics and outcome in cirrhotic patients with portal hypertension is unknown. We analyzed the levels of miRNA-34a in cirrhotic patients with severe portal hypertension.

Methods

We included 60 cirrhotic patients receiving TIPS for prevention of rebleeding and/or therapy-refractory ascites. miRNA-34a levels were measured using qPCR and normalized by SV-40 in the portal and hepatic venous blood of these patients taken at TIPS procedure. Hemodynamic and clinical parameters were assessed before TIPS and during follow-up.

Results

Levels of miRNA-34a were higher in the hepatic vein than in the portal vein. Circulating miRNA-34a in the hepatic vein correlated with ALT, CHE and sodium excretion after TIPS. miRNA-34a showed no correlation with portal pressure, but its levels in the portal vein correlated inversely with the congestion index. Interestingly, the levels of miRNA-34a in the portal and hepatic vein showed inverse correlation with arterial pressure. Furthermore, levels of miRNA-34a in the hepatic vein had a predictive value for survival, but MELD, creatinine at short-time follow-up 14 days after TIPS-insertion and portal pressure after TIPS performed better.

Conclusion

This study demonstrates for the first time, that miRNA-34a may originate to a large extent from the liver. Even though higher levels of miRNA-34a are possibly associated with better survival at long-term follow-up in cirrhotic patients with severe portal hypertension receiving TIPS, classical prognostic parameters predict the survival better.     

Trafficking of natural killer cells

Natural killer (NK) cells comprise a set of lymphocytes that is capable of mediating innate immune responses to viral infections, malignancies, and allogeneic bone marrow grafts. This review summarizes what is known about the mechanisms NK cells use to arrive at their sites of action. NK cells express a wide array of adhesion molecules including alphaLbeta2, alphaMbeta2, alphaXbeta2, and alpha4beta1 integrins, ICAM-1, PSGL-1, and L-selectin. Like other immune and inflammatory cells, NK cells use the blood circulation to enter tissues and organs, which requires that they interact with the vessel wall under flow conditions, arrest, and transmigrate. NK cells are able to chemotax to a variety of cytokines and chemokines, including IL-12, IFN-(alpha/beta, CCL2, 3, 4, 5, 7, 8, CXCL8, and CX3CL1. In many cases, NK cells appear to migrate towards these soluble factors without any kind of priming. These cells also appear to distribute in secondary and tertiary lymphoid sites (i.e., spleen, bone marrow, liver, lung, and lymph nodes) both with and without stimulation. In addition to their ability to move throughout the body in an unprimed state, activated NK cells may have increased specificity in homing to sites of inflammation. NK cells not only react to, but also produce IFN-gamma, TNF-alpha, GM-CSF, CCL3, CCL4, and CCL5, enabling them to recruit various immune cells to sites of immune response.     

肝硬化患者肝脏门静脉血流与肝叶萎缩之间关系的研究

目的：探讨肝硬化患者肝脏右叶、左叶体积变化,检测肝硬化患者门静脉血流情况,分析二者之间的关系,以及门静脉血流与肝功能之间关系。方法：本研究纳入54例肝硬化患者和40例正常人,采用超声多普勒方法分析这些受试者的肝脏体积和门静脉主干及左右分支的内径、血流速、流量数据,并通过静脉血检测白蛋白、胆红素、胆碱酯酶水平等评估患者肝功能水平。结果：肝硬化组平均年龄46.3岁,男性32例,其中childA级患者16例,childB级患者27例,childC级患者11例;正常对照组平均年龄41．8岁,男性24例。肝硬化组患者右左肝叶之比明显低于正常对照组（p〈0．05）,门静脉内径和血流量明显高于正常对照组（p〈0．05）．随着child分级升高,门静脉血流量也明显升高。肝硬化组门静脉右支血流量明显低于左支血流量（p〈0．05）;此外肝硬化患者门静脉右支和左支血流量之比明显低于正常人群门静脉右左支之比（p〈0．05）;而且肝硬化患者门静脉右左支血流量之比与右左肝叶具有明显的相关性与右左肝叶之比具有明显的相关性（r=0．64,p〈0．05）。结论：评估肝硬化病人门静脉血流情况,对于判断肝脏病理变化程度,评价治疗效果,以及选择治疗方案方面都具有重要的临床价值     

Lymphocyte-fibroblast adhesion induced by interferon-gamma

Adhesion of lymphocytes to vascular endothelium is thought to be of importance in regulating the passage of lymphocytes from the circulation to areas of inflammation. Evidence suggests the presence of site-specific lymphocyte receptor molecules on the endothelial cell surface which can be modulated by soluble immune factors. The factors responsible for maintaining lymphocyte infiltration at tissue sites are unknown. We have examined the adherence of human peripheral blood T lymphocytes to human fibroblast monolayers in vitro and the role of interferon-gamma in enhancing adherence. Treatment of fibroblasts with interferon-gamma resulted in an increase in the number of adherent T cells in a dose- and time-dependent manner. Enhanced adhesion was noted as early as 4 hr after interferon stimulation (291 +/- 7 T cells/field vs 51 +/- 10 without IFN stimulation) and binding was further increased by lengthening the exposure time of fibroblasts to interferon up to 72 hr (475 +/- 86 T cells/field). Kinetic and inhibition experiments using monoclonal antibody to HLA-DR demonstrated that adhesion of T lymphocytes to interferon-stimulated fibroblasts proceeds by a mechanism independent of DR induction. In addition, adherence was not histocompatibility antigen-restricted, as adherence to autologous and allogeneic fibroblast monolayers was not significantly different. Nonadherent T cells, collected at the end of adhesion assays, were deficient in their capacity to bind to a second interferon-treated monolayer, suggesting the depletion of a subpopulation of T cells responsible for adhesion. Alterations of fibroblasts in vivo by immune cell-derived cytokines may be an important mechanism for the localization of lymphocytes at sites of connective tissue inflammation.     

Gamma delta TCR cells in hepatic sinusoids and intestinal intraepithelia

We provided here the conception that the liver is an important immune organ after birth. On the other hard, it is well established that the liver in the fetal stage works as a hematopoietic organ. Although a significant number of gamma delta TCR cells are distributed in epithelia of the skin, intestine and reproductive organs, the liver is also one of the most predominant organs of gamma delta TCR cells. The percentages of gamma delta TCR cells in MNC of hepatic sinusoids increased up to 16.0% in young mice aged 4 wk, and approximately 40% of such gamma delta TCR cells expressed the CD8 antigens. V gene segment usage analysis by the PCR method demonstrated that a unique set of V gamma 2/V delta 6 was preferentially used by hepatic gamma delta TCR cells. The predominant appearance of unique gamma delta TCR cells in hepatic sinusoids of mice, including nude mice, proposed us the possibility that these gamma delta TCR cells may differentiate non-thymus dependently in the liver. The lymphocytes in the hepatic sinusoids may be intimately related to the antigens come from the intestine and to the lymphocytes sensitized there. Therefore, we introduced recent evidences about gamma delta T cells in the intestine and discussed their connection with the hepatic gamma delta T cells.     

In vivo uptake of ethanol and release of acetate in rat liver and GI

The concentration gradients of ethanol and acetate across liver and Gl were determined in overnight starved rats infused with ethanol at a rate (15 μmol/min/rat) below and a rate (30 μmol/min/rat) exceeding the rate of ethanol disposal in the animals. Plasma concentrations of ethanol in the systemic circulation reached steady-state levels of ∼0.6 mM between 30 and 60 min during low rate of infusion; increased steadily from 3.5 mM at 30 min to 6.4 mM at 2 h during high rate of infusion. Gl metabolism was determined by concentration differences in aorta and portal vein; hepatic metabolism by differences in hepatic influx and hepatic veins. Hepatic influx was the sum of the concentrations in aorta and portal vein, each multiplied by their fractional contributions to heoatic blood supply. At low rate of infusion, hepatic extraction of ethanol was nearly complete and could be accounted for entirely by the acetate released from liver. The concentrations of ethanol in aorta were greater but not significantly than that in portal vein. At high rate of infusion, hepatic and Gl gradients of ethanol remained constant despite changes in circulating concentrations of ethanol. The concentration gradients of ethanol and acetate across liver, though different in signs, were identical in magnitude. Gl gradient indicating uptake of ethanol was statistically significant and was about 30 % of hepatic gradient. Enzyme activity of alcohol dehydrogenase in stomach was found to be about 10 % of that in liver. Our results thus show that acetate generated during ethanol oxidation is completely released from liver in rats, in either conscious or anesthetized state under submaximal or maximal condition of ethanol disposal, and that Gl metabolism of circulating ethanol can be as high as one third of the metabolism in liver.     

Visualization and Analysis of Blood Flow and Oxygen Consumption in Hepatic Microcirculation: Application to an Acute Hepatitis Model

There is a considerable discrepancy between oxygen supply and demand in the liver because hepatic oxygen consumption is relatively high but about 70% of the hepatic blood supply is poorly oxygenated portal vein blood derived from the gastrointestinal tract and spleen. Oxygen is delivered to hepatocytes by blood flowing from a terminal branch of the portal vein to a central venule via sinusoids, and this makes an oxygen gradient in hepatic lobules. The oxygen gradient is an important physical parameter that involves the expression of enzymes upstream and downstream in hepatic microcirculation, but the lack of techniques for measuring oxygen consumption in the hepatic microcirculation has delayed the elucidation of mechanisms relating to oxygen metabolism in liver. We therefore used FITC-labeled erythrocytes to visualize the hepatic microcirculation and used laser-assisted phosphorimetry to measure the partial pressure of oxygen in the microvessels there. Noncontact and continuous optical measurement can quantify blood flow velocities, vessel diameters, and oxygen gradients related to oxygen consumption in the liver. In an acute hepatitis model we made by administering acetaminophen to mice we observed increased oxygen pressure in both portal and central venules but a decreased oxygen gradient in the sinusoids, indicating that hepatocyte necrosis in the pericentral zone could shift the oxygen pressure up and affect enzyme expression in the periportal zone. In conclusion, our optical methods for measuring hepatic hemodynamics and oxygen consumption can reveal mechanisms related to hepatic disease.     

Splanchnic glucagon kinetics in exercising alloxan-diabetic dogs.

The purpose of this study was to define the relationship between arterial immunoreactive glucagon (IRG) and IRG that perfuses the liver via the portal vein during exercise in the diabetic state. Dogs underwent surgery >16 days before the experiment, at which time flow probes were implanted in the portal vein and the hepatic artery, and Silastic catheters were inserted in the carotid artery, portal vein, and hepatic vein for sampling. Dogs were made diabetic with alloxan injected intravenously approximately 3 wk before study (AD) or were studied in the nondiabetic state (ND). Each study consisted of a 30-min basal period and a 150-min moderate-exercise period on a treadmill. The findings from these studies indicate that the exercise-induced increment in portal vein IRG can be substantially greater in AD compared with ND, even when arterial and hepatic vein increments are not different. The larger IRG gradient from the portal vein to the systemic circulation in AD dogs is a function of a twofold greater increase in nonhepatic splanchnic IRG release and a fivefold greater hepatic fractional IRG extraction during exercise. In conclusion, during exercise, arterial IRG concentrations greatly underestimate the IRG levels to which the liver is exposed in ND, and this underestimation is considerably greater in dogs with poorly controlled diabetes.     

不同入肝血流阻断方式对荷瘤小鼠肝功能影响的实验研究

目的:探讨不同血流阻断方式对荷瘤小鼠肝细胞功能的影响。方法:选择昆明小鼠24只随机分为三组,正常对照组(Suspe-nded operation,SO)、肝门阻断组(Occlusion of the portal triad,OPT)、保留肝动脉持续阻断门静脉(Occlusion of portal vein,OPV)各8只。采用门静脉注射肿瘤的方法建立肝癌模型,建模后3天采用阻断范围为左外叶和中叶、阻断时间为60分钟的入肝血流阻断方式,复流后5天后,通过测量3组对肝脏的缺血再灌注损伤程度以及病理学变化来评价不同血流阻断方式对肝细胞功能影响的程度。结果:门静脉注射小鼠肝癌细胞8天后,对照组测量小鼠正常丙氨酸氨基转移酶(ALT)值为66.5±22.3 IU/L,OPT组值为276.3±80.5 IU/L,OPV组值为89.6±28.4 IU/L,两组比较有统计学差异(P0.01);对照组测量小鼠正常天冬氨酸氨基转移酶(AST)值为301.3±126.7 IU/L,OPT组值为1126.4±285.5 IU/L,OPV组值为438.6±150.7 IU/L,两组比较有统计学差异(P0.01),病理组织学OPV组肝细胞损伤程度明显较OPT组轻。结论:保留肝动脉持续阻断门静脉可以减轻荷瘤小鼠肝脏的缺血再灌注损伤。