Hepatic artery versus portal vein and systemic infusion of fluorodeoxyuridine of rabbit VX-2 hepatic implants

To compare the efficacy of regional and systemic infusions of hepatic tumors, and to correlate this with tumor perfusion, 29 New Zealand white rabbits underwent perfusion of VX-2 hepatic implants. Tritium-labeled fluorodeoxyuridine (H3-FUDR) and technetium-99m-labeled macroaggregated albumin (Tc 99m-MAA) were infused through the hepatic artery, portal vein, and peripheral vein. Hepatic artery infusion resulted in a significantly improved tumor-to-liver ratio of FUDR uptake (p less than 0.001). The increased tumor uptake correlated with a two-fold increase in tumor arterial blood flow as compared with normal liver demonstrated by the MAA infusion. We conclude that infusional therapy is superior to both portal vein and systemic infusions. Portal vein infusion results in no uptake of drug by the tumor. Hepatic artery scintigraphy with MAA may be useful in selecting appropriate patients for this type of therapy.     

Human Serum Albumin Microspheres Approximate Initial Organ-Specific Biodistributions of Transplanted Hepatocytes and Are Effective Cell Surrogates for Safety Studies

Liver repopulation with transplanted hepatocytes will generate novel cell-based therapies, although translocation of transplanted cells into lungs through portasystemic shunts has the potential for embolic complications. To facilitate safety analysis of hepatocyte transplantation, we wished to obtain effective cell surrogates and analyzed biodistributions of similarly sized ^99mTc-labeled human serum albumin microspheres and rat hepatocytes. Image analysis with dual ^99mTc and ¹¹¹In labels indicated that cells and microspheres were similarly distributed in the liver when injected into normal rats via the spleen. Also, their distributions were similar when injected via a femoral vein or the superior mesenteric vein with cells and microspheres localizing in lungs or liver, respectively. Upon intraportal injection in rats with portal hypertension, microspheres localized in both liver and lungs, consistent with portasystemic shunting. These data demonstrate that human serum albumin microspheres are effective cell surrogates for approximating the safety of hepatocyte transplantation and should be clinically useful.     

Predicting tumor response in patients with colorectal hepatic metastases.

Until now, there has been no reliable means of predicting tumor response to chemotherapy in patients with metastatic colorectal cancer. Using arterial nuclide flow scans as a determinant of tumor response, the degree of tumor perfusion was evaluated in a blinded prospective study. Seventy-three patients with colorectal hepatic metastases received continuous hepatic arterial (N = 52) or systemic intravenous (N = 21) chemotherapy using an implantable pump. All patients had pretreatment hepatic arteriography and arterial flow scans using 99mTc macroaggregated albumin (99mTc-MAA). An arteriogram was characterized as positive if it showed tumor hypervascularity; the 99mTc-MAA flow scan was considered positive if it showed increased tumor uptake relative to the liver. Of 47 patients with an evaluable 99mTc-MAA flow scan who were treated with arterial infusion, 31 had a positive scan; in this group 16 responded to chemotherapy. The 99mTc-MAA scan was negative in 16 patients, of whom one responded to chemotherapy (p less than 0.006). The 99mTc-MAA scan had the greatest predictive value in previously untreated patients (sensitivity = 91%; specificity = 77%). The arteriogram was positive in 25 of 46 evaluable patients, but this finding had little predictive value for tumor response (sensitivity = 56%; specificity = 46%). Of 21 patients receiving systemic intravenous infusion, the scan was positive in nine patients, of whom seven responded to chemotherapy. The 99mTc-MAA scan was negative in 12 patients, of whom one responded to chemotherapy (sensitivity = 88%; specificity = 85%). When 99mTc-MAA-positive and -negative groups were compared, there were no differences in mean patient age, per cent liver involvement, tumor size, or plasma liver function tests. Hepatic tumor perfusion as determined by MAA arterial flow scan is a reliable predictor of tumor response in patients with metastases from large bowel cancer. The test provides a valuable criterion for selecting individuals for treatment of metastases from large bowel cancer by infusion chemotherapy.     

A Novel Method of Determining Portal Systemic Shunting using Biodegradable TC Labelled Albumin Microspheres

Portal systemic shunting (PSS) and portal pressure were measured in control rats and in animals with portal hypertension induced by partial portal vein ligation (PPVL). The portal pressure in rats with partial portal vein ligation (13.4 +/- 0.5 mm.Hg.) was significantly higher (p < 0.005) than in the control group (9.6 +/- 0.6 mm.Hg.). Portal systemic shunting measured by consecutive injections of radiolabelled methylene diphosphonate (MDP), a non-diffusable marker and albumin microspheres directly into the splenic pulp was significantly increased (P < 0.005) in the portal hypertensive animals (30.8 +/- 2.5%) compared to sham operated rats (2.6 +/- 1.5%). Similarly, in portal hypertensive rats portal systemic shunting measured by intrasplenic injections of radiolabelled cobalt microspheres (37.1 +/- 3.9%) was significantly greater (p < 0.005) than in control animals. There was a good correlation and agreement (r = 00.97) between the two methods of measuring portal systemic shunting. However because the (99)Tc(m)-albumin microspheres are biodegradable the method allows portal systemic shunting to be measured in man. Furthermore since the computer adjusts the baseline to zero after each determination of portal systemic shunting the methodology allows repeated measurements to be made.     

Evidence for role of prostacyclin as a systemic hormone in portal hypertension

The possibility that prostacyclin could be a systemic hormone and could mediate the splanchnic hyperemia of chronic portal hypertension was evaluated in rabbits in a normotensive state and in rabbits with chronic partial ligation of the portal vein. In rabbits with portal hypertension (PHT), 6-keto-prostaglandin F1 alpha (PGF1 alpha, a prostacyclin degradation product) was elevated twofold in all vascular beds (systemic arterial, systemic venous, and portal venous) when compared with levels in control animals. In PHT rabbits, exogenous prostacyclin infusion after cyclooxygenase blockade through the systemic arterial, systemic venous, or portal venous route resulted in an equal elevation of 6-keto-PGF1 alpha in the reciprocal vascular beds and restored the original precyclooxygenase blockade hemodynamics. These hemodynamic changes were of equal magnitude irrespective of site of infusion in PHT. In controls there was no significant change in 6-keto-PGF1 alpha or hemodynamics with intraportal infusion. We conclude that prostacyclin achieves systemic levels by escaping hepatic degradation resulting from portosystemic shunting in the animal with chronic portal hypertension.     

应用硝普钠促进经门静脉移植的骨髓间充质干细胞在肝内弥散分布

目的探讨硝普钠是否可促进经门静脉移植的骨髓间充质干细胞(MSCs)在肝内弥散分布。方法分离SD大鼠的骨髓MSCs,进行培养、传代,流式细胞仪鉴定MSCs表面标记,以Fe2O3-PLL标记供移植的MSCs。以彩色多普勒超声检查大鼠注射硝普钠后10～20 min时门静脉内径及血流速度变化,并计算其血流量。受者(SD大鼠)背部皮下注射四氯化碳,制成肝损伤模型,将模型随机分为实验组和对照组,实验组经门静脉注射以Fe2O3-PLL标记的MSCs悬液0.5 ml及含硝普钠的生理盐水(硝普纳的注入量为24 nmol/100g),对照组仅注射Fe2O3-PLL标记的MSCs悬液0.5 ml。分别于MSCs注射前及注射后3 h、1周、2周、4周行磁共振扫描,测定肝脏信噪比(SNR)。最后1次磁共振扫描后,处死全部受者,取各叶肝组织,行HE染色和普鲁士蓝染色,进行组织学观察。结果分离获得的MSCs经培养、传代,高表达CD29(99.88%)和CD90(99.84%),CD45阳性细胞极少(0.13%)。注射硝普钠后10～20 min,大鼠门静脉内径明显扩张(P<0.01),门静脉血流量明显增多(P<0.01)。移植后随着时间延长,两组肝脏SNR均逐渐增高,实验组移植后3 h、1周、2周时的肝脏SNR明显低于对照组(P<0.05),至移植后4周,两组肝脏SNR的差异无统计学意义;两组移植后3 h、1周、2周时的肝脏SNR均明显低于移植前(P<0.05),至移植后4周,肝脏SNR恢复至移植前水平。实验组肝组织普鲁士蓝染色阳性细胞多于对照组(P<0.01)。结论门静脉注入硝普钠后,其分支内径扩大,血流量增加,在经门静脉移植MSCs的同时注入硝普钠可促进MSCs向末梢分支与血窦弥散分布。     

Hepatocyte transplantation through the hepatic vein: a new route of cell transplantation to the liver

The efficiency of hepatocyte transplantation into the liver varies with the method of administration. This study investigated whether retrograde infusion via the hepatic vein provides a sufficient number of donor cells for the liver. Donor hepatocytes were isolated from dipeptidyl peptidase IV (DPPIV(+)) rats and transplanted into DPPIV(-) rat livers either by antegrade portal vein infusion or retrograde hepatic vein infusion. Hepatocyte engraftment ratios and localization were evaluated by histological DPPIV enzymatic staining at 1 week and 8 weeks after the transplantation. No significant differences in engraftment efficiency were observed at either 1 week or 8 weeks after transplantation by either route. However, the localization of the transplanted hepatocytes differed with the administration route. Portal vein infusion resulted in predominantly periportal engraftment, whereas hepatic vein infusion led to pericentral zone engraftment. Immunohistochemical analysis showed that the transplanted hepatocytes engrafted in the pericentral zone after retrograde infusion displayed intense CYP2E1 staining similar to the surrounding native hepatocytes. CYP2E1 staining was further enhanced by administration of isosafrole, an inducing agent for various cytochrome P450 enzymes, including CYP2E1. This study demonstrates a novel approach of transplanting hepatocytes into the liver through retrograde hepatic vein infusion as the means to target cell implantation to the pericentral zone.     

自体骨髓移植治疗失代偿期肝硬化的临床观察

目的 研究自体骨髓经门静脉输注对失代偿期肝硬化的治疗作用。方法 回顾性分析2016年1月到2019年12月对失代偿期肝硬化患者做自体骨髓经门静脉输注的临床资料。其中30例进行常规药物保肝利尿等治疗,52例常规治疗+自体骨髓经门静脉输注,55例常规治疗+脾切除+自体骨髓经门静脉输注。结果 30例进行常规治疗后1个月和3个月与治疗前相比肝功能和血常规各项指标没有好转;2例死于消化道出血。52例常规治疗+门静脉自体骨髓输注治疗后1个月和3个月肝功能指标明显好于常规治疗（P＜0.05）;2例死于消化道出血。55例常规治疗+脾切除+自体骨髓经门静脉输注治疗后1和3个月肝功能指标明显好于常规治疗（P＜0.05）;3例手术后1周内死于创面出血诱发的肝衰竭。治疗3个月后,常规治疗+脾切除+自体骨髓经门静脉输注、常规治疗+自体骨髓经门静脉输注与常规治疗相比,在白细胞数[（6.28±1.63）×10⁹,（3.39±0.98）×10⁹,（3.04±0.65）×10⁹]、血红蛋白量[（107.16±19.25）g/L,（98.66±19.81）g/L,（92.54±17.52）g/L]、血小板数[（223.00±47.99）×10⁹,（45.52±12.93）×10⁹,（38.64±9.48）×10⁹]方面均明显增高（P＜0.05）。结论 常规治疗对失代偿期肝硬化没有明显疗效。常规治疗加自体骨髓经门静脉输注可以明显促进失代偿期肝硬化的肝功能重建,但是不能缓解脾功能亢进。脾切除加自体骨髓经门静脉输注可以解除脾功能亢进,并促进失代偿期肝硬化的肝功能重建,但是脾切除术后创面渗血容易诱发肝衰竭,有较高手术风险。对肝功能C级的失代偿期肝硬化可以先作上腹部小切口经网膜右静脉插管输注自体骨髓,待肝功能好转后,再做脾切除,可以降低手术风险。     

Reconstruction of the portal vein using a peritoneal patch-graft

BACKGROUND: Reconstruction of the portal vein with autologous veins requires extra incisions. Prosthetic material is associated with an increased risk of infection. We therefore created an animal model of portal vein reconstruction using the peritoneum. METHODS: A 2.5 x 2.5 cm piece of the peritoneum was resected from Landrace pigs weighing 30 to 40 kg and was dipped in 100% alcohol for 10 minutes. The anterior wall of the portal vein measuring 1.2 x 0.6 cm was resected. The peritoneal patch-graft fitting the defect of the portal vein was used to repair it. RESULTS: All 7 pigs survived the surgery, and were killed at 2, 7, 7, 14, 21, 35 and 49 days, respectively, after surgery. There was no evidence of thrombosis or obstruction of the reconstructed portal vein or any other complications. Complete endothelialization of the patches were noted at day 14. CONCLUSIONS: Our patch-graft technique using the peritoneum is considered to be a good and safe alternative for reconstruction after partial resection of the portal vein in clinical surgery.     

Intraportal hepatocyte transplantation in the pig: hemodynamic and histopathological study

BACKGROUND: Hepatocyte transplantation is an attractive treatment for various liver diseases. The intraportal route of transplantation is favored, but little information is available on the possible adverse effects in this technique. We investigated the influence of intraportal loads of hepatocytes on portal, pulmonary, and systemic hemodynamics in 13 pigs. METHODS: Under general anesthesia, pigs were provided with an arterial line, a Swan-Ganz catheter, and two intraportal catheters, one for cell infusion and one for heparin infusion and portal pressure measurement. Pig hepatocytes were infused at a rate of 25 million cells/min. RESULTS: The first six animals were used to develop the infusion technique. In the last seven animals, portal pressure increased linearly with cell load upon infusion of 400-2400 x 10(6) hepatocytes (r(2)=0.704;P<0.05). Portal flow measured by Doppler sonography decreased by 23-66% below basal values. An inverse linear relationship was found between portal pressure and portal flow (r(2)=0.679; P<0.05), portal flow approaching zero for portal pressure >40 mmHg. Pulmonary arterial pressure increased by 11-62%. AST increased up to 10-fold, and platelets decreased by 22-58%. Hepatocytes-containing thrombi were present in segmental and in smaller portal branches. Hepatocytes were always identified in lung sinusoids 48 hr after infusion, and a small basal pulmonary infarction was found in one animal. CONCLUSION:. These data suggest that up to 2.4% of total hepatocyte mass can be infused in this large animal model. However, the risk of significant thrombotic complications should be considered for clinical applications.     

Establishment of practical recellularized liver graft for blood perfusion using primary rat hepatocytes and liver sinusoidal endothelial cells

Tissue decellularization produces a three‐dimensional scaffold that can be used to fabricate functional liver grafts following recellularization. Inappropriate cell distribution and clotting during blood perfusion hinder the practical use of recellularized livers. Here we aimed to establish a seeding method for the optimal distribution of parenchymal and endothelial cells, and to evaluate the effect of liver sinusoidal endothelial cells (LSECs) in the decellularized liver. Primary rat hepatocytes and LSECs were seeded into decellularized whole‐liver scaffolds via the biliary duct and portal vein, respectively. Biliary duct seeding provided appropriate hepatocyte distribution into the parenchymal space, and portal vein–seeded LSECs simultaneously lined the portal lumen, thereby maintaining function and morphology. Hepatocytes co‐seeded with LSECs retained their function compared with those seeded alone. Platelet deposition was significantly decreased and hepatocyte viability was maintained in the co‐seeded group after extracorporeal blood perfusion. In conclusion, our seeding method provided optimal cell distribution into the parenchyma and vasculature according to the three‐dimensional structure of the decellularized liver. LSECs maintained hepatic function, and supported hepatocyte viability under blood perfusion in the engineered liver graft owing to their antithrombogenicity. This recellularization procedure could help produce practical liver grafts with blood perfusion.     

Simultaneous segmental obstruction of bile duct and portal vein markedly changes a population of biliary and hepatic cells in human liver

BACKGROUND AND AIMS: No studies have investigated histologic changes caused by simultaneous segmental obstruction of the bile duct and portal vein in human liver. PATIENTS/METHODS: Liver tissues with simultaneous obstruction of the segmental bile duct and portal vein (O(+/+) liver), with segmental bile duct obstruction alone (O(+/-) liver), and without obstruction (O(-/-) liver) were obtained from patients who underwent hepatectomy, and studied morphologically and immunohistochemically. RESULTS: In O(+/+) liver, the proportional area consisting of hepatocytes was significantly less (31.0+/-25.8%) than in O(+/-) liver (78.4+/-18.9%) or O(-/-) liver (86.5+/-9.2%). In contrast, the proportional area consisting of biliary epithelial cells was significantly higher in O(+/+) liver (9.1+/-6.1%) than in O(+/-) liver (1.6+/-1.5%) or O(-/-) liver (0.7+/-0.6%). The proportional area consisting of fibrous tissue also was significantly higher in O(+/+) liver than in the other two groups. In O(+/+) liver, some cells located at the periphery of hepatocyte areas were immunoreactive for both hepatocyte and biliary epithelial cell markers. CONCLUSION: Simultaneous segmental obstruction of the bile duct and portal vein induces a marked ductular increase, periportal fibrosis, and a reduction in the number of hepatocytes in human liver tissue.     

Inferior mesenteric venous left renal vein shunting for decompression of excessive portal hypertension in adult living related liver transplantation

In the present study, we investigated the effect of decompression of excessive portal hypertension by inferior mesenteric venous (IMV) left renal vein shunting in 7 cirrhotic patients with esophago-gastric varices and 2 patients who underwent adult living related donor liver transplantation (ALRDLT). The portal pressure remarkably decreased after shunting in all patients with esophago-gastric varices (388 ± 42 mm H₂O vs. 247 ± 57 mm H₂O; P < .05). It also decreased after a shunt operation in patients who had undergone liver transplantation. We report that the excessive shear stress by portal hypertension after small-for-size LRDLT induces a liver injury and the decompression of portal hypertension by splenic arterial ligation or splenectomy prevents postoperative liver injury following massive hepatectomy and small-for-size LRDLT. Our present studies suggested that IMV left renal vein shunting might prevent postoperative liver injury by partial decompression of excessive portal hypertension following small-for-size LRDLT.     

Hepatic artery vs. portal vein infusion of microbeads: a large animal pre‐clinical model evaluating the intrahepatic capacity for cell infusion and imaging

Wang W, Liu S, Zheng W, Gao F, Hawthorne WJ, Yi S. Hepatic artery vs. portal vein infusion of microbeads: a large animal pre‐clinical model evaluating the intrahepatic capacity for cell infusion and imaging. Xenotransplantation 2010; 17: 207–214. © 2010 John Wiley & Sons A/S. Abstract: Background: Islet xeno‐transplantation via the portal vein has been proposed as an alternative of islet allo‐transplantation for treatment of type 1 diabetes. However, the precise hepatic capacity has not been addressed. Methods: We mimicked cell transplantation by infusion of dogs with alginate/poly‐1‐lysine/alginate (APA) microbeads via either the portal vein (PV) or hepatic artery (HA). The maximal adaptable capacity for infused microbeads was evaluated by examination of vasculature, microvasculature, hepatic hemodynamics, portal vein, and hepatic artery pressures and liver function in the microbead recipient dogs. Results: PV but not HA dogs demonstrated elevated portal pressure during the infusion procedure in a dose‐dependent manner. Four out of twelve PV dogs infused with 32 000 microbeads/kg developed acute liver infarction within 24 h after infusion with four of the remaining eight animals developing portal venous thrombosis within 24 h following infusion. All PV animals demonstrated abnormal alanine aminotransferase (ALT) values, and the extent and duration of increased ALT levels correlated with the increase in the number of microbeads infused. In contrast, HA animals infused with as many as 32 000 microbeads/kg had neither portal thrombosis nor abnormal liver function. Conclusions: The capacity for intrahepatic cell infusion is finite and the intrahepatic artery may have a less hemodynamic interference impact on transplantation of cells into the liver when a larger volume of cells is required to achieve curable outcomes in both allo‐ and xeno‐transplantation.     

Hepatopedal flow restoration in patients intolerant of total portal diversion.

This report describes an experience with operative restoration of hepatopedal portal blood flow in five patients intolerant of total splanchnic shunting. Portal flow was reestablished by takedown of the total shunt and construction of a selective, distal splenorenal shunt, or by isolation and arterialization of the hepatic limb of the shunted portal vein. In two patients, shunt revision was undertaken electively for chronic encephalopathy, which had been unresponsive to low-protein diet, intestinal antibiosis and oral lactulose. Eighteen and 48 months after operation, both patients have had no encephalopathy on an unrestricted protein intake, and work actively as homemakers. Needle liver biopsies showed enhanced mitotic activity in the early postoperative period, suggesting hepatocyte regeneration. In three patients, shunt conversion or arterialization was undertaken in desperate circumstances, characterized by liver failure (bilirubin greater than 10 mg/dl, albumin less than 2.5 g/dl, prothrombin time greater than 16 sec), coma, and respirator dependency. Although the patients showed immediate, marked improvement in mentation, all three died of intraabdominal hemorrhage in the first few postoperative days, in spite of maximum blood product support. Two conclusions can be drawn from this limited experience: (1) at a time of election, restoration of hepatopedal portal flow can be accomplished with considerable benefit in patients with side-to-side portacaval or hemodynamically equivalent shunts, and (2) similar procedures in patients with fulminant liver failure are unlikely to succeed.     

Postshunt encephalopathy in liver transplanted children with portal vein thrombosis

BACKGROUND: Surgical portosystemic shunting has been reported to alleviate successfully portal hypertension in liver transplanted recipients with portal vein thrombosis. METHODS: We report two liver transplanted children with portal vein thrombosis who developed post-shunt acute encephalopathy. In one child, a mesocaval H-type shunt was created surgically because of bleeding related to Roux-en-Y loop varices at 3 months posttransplantation; in the other, a large spontaneous splenorenal shunt was discovered at the time of diagnosis of portal vein thrombosis on day 34 posttransplantation and was preserved. RESULTS: Post-shunt encephalopathy developed 6 months and 2.7 years after transplantation, causing death in one child. CONCLUSIONS: This report illustrates the risk and the possible dismal outcome of post-shunt encephalopathy in liver transplanted children. Therapeutic procedures other than portosystemic shunting that will restore an hepatopetal portal flow to the liver graft should be considered in liver-transplanted children with portal vein thrombosis.     

Living related liver transplantation in children with hypoxemia related to intrapulmonary shunting

Abstract  Living related liver transplantation (LRLT) was performed in seven children with hypoxemia related to intrapulmonary shunting. Based on the degree of the shunt ratio calculated by technetium ⁹⁹m macroaggregated albumin (MAA) scintigraphy, the seven patients were classified in the moderate (shunt ratio under 40 %, n = 4) or severe group (shunt ratio over 40 %, n = 3). While Pa was maintained over 60 mmHg in the moderate group, that in the severe group continued at a low level of under 40 mmHg in the early postoperative period. However, 48 h after surgery the arterial ketone body ratio recovered to a safe level of 1.0 in both groups. Values of aspartate aminotransferase and serum total bilirubin decreased at a constant rate in both groups. Six patients survived, but one died of portal vein thrombosis on the 53 rd postoperative day. Five of six surviving patients recovered from hypoxemia. We concluded that the transplanted liver can tolerate the stress of severe hypoxemia after LRLT.     

腹腔镜结直肠癌根治术并脐静脉置泵化疗预防术后肝转移的临床研究

目的:研究腹腔镜结直肠癌根治术后经脐静脉化疗泵持续灌注5-FU对减少术后肝转移、提高远期疗效的作用.方法:为106例患者行腹腔镜结直肠癌根治术,随机分为脐静脉化疗组(研究组,n =53)和对照组(n=53).研究组术中经脐静脉向门静脉插管,术后即从脐静脉化疗泵持续给予5-FU 1g/d,连续7d.对比分析两组近期并发症...     

The effect of intraportal prostaglandin E1 on adhesion molecule expression, inflammatory modulator function, and histology in canine hepatic ischemia/reperfusion injury

BACKGROUND: Prostaglandin E1 (PGE1) is known to protect the liver from I/R, however, the mechanism of cytoprotection is not well understood. This study investigates the effect of intraportal infusion of PGE1 in a warm liver ischemia/reperfusion (I/R) model on cytokines, adhesion molecules and liver structure. MATERIALS AND METHODS: Twenty dogs underwent laparotomy under general anesthesia. PGE1 (0.02 microg\kg\min) was perfused through the portal vein in the PGE1 group (n = 10), or a similar volume of Ringer's solution in the control group (n = 10) for 15 min. Liver ischemia was induced by hepatic artery and portal vein occlusion and PGE1 was infused via the portal vein for 60 min. The occlusion was released and PGE1 infusion recommenced for 30 min. Blood and liver biopsies were sampled at baseline, 60 min ischemia, and 30 min reperfusion and assessed for transaminases, cytokines, adhesion molecules, and electron microscopy. RESULTS: PGE1 infusion significantly reduced transaminases TNF-alpha, sICAM-1, sP-selectin, and sE-selectin on ischemia and reperfusion. PGE1 reduced hepatocytic degeneration, portal and central ICAM-1 expression, central and sinusoidal VCAM-1 expression, portal and central P-selectin expression, and portal and sinusoidal E-selectin expression on reperfusion. CONCLUSION: Intraportal PGE1 infusion reduced I/R injury and was associated with down-regulation of ICAM-1, VCAM-1, P-selectin, and E-selectin on reperfusion.