Heterotopic liver transplantation in rats: effect of intrahepatic islet isografts and split portal blood flow on liver integrity after auxiliary liver isotransplantation

BACKGROUND: Auxiliary heterotopic liver grafts atrophy in the absence of portal venous inflow; evidence suggests that an islet-derived hepatotrophic factor may exist in the portal drainage. Here we examine the effects of intrahepatic islet isografts in maintaining hepatocyte integrity in Wistar Furth rats with one of several types of arterialized auxiliary liver isografts. METHODS: In type 1 procedures the auxiliary liver was interposed into the recipient infrarenal vena cava and perfused through the graft portal vein with caval blood. In type 2 procedures the donor infrahepatic vena cava was anastomosed end-to-side to the recipient vena cava and the recipient portal vein was diverted to the graft portal vein. Both types of auxiliary grafts were arterialized; bile duct drainage was through the duodenum. Syngeneic islets were isolated and embolized into the portal veins of one half of the donor type 1 or native type 2 livers (1500 to 1700 islets). Finally, we performed six type 3 procedures in which a type 2 procedure was performed except that the portal blood flow was split so that the portal vein receiving the splenic, gastric, pancreatic, and duodenal drainage supplied the native liver and that the common mesenteric vein supplied the auxiliary graft with equivalent portal blood flow. Atrophy in heterotopic and native livers were compared for the three models after 3 months. RESULTS: Intrahepatic islets in type 1 auxiliary liver isografts without portal venous inflow did not prevent graft atrophy. Conversely, native livers deprived of portal venous inflow in our type 2 procedures, regardless of the presence of intrahepatic islet isografts, atrophied relative to auxiliary liver grafts in which portal venous inflow was provided by diverting the recipient's portal vein to the graft. In type 3 recipients atrophy was greater in the native livers than in the grafts. CONCLUSIONS: The results of our study suggest that islet-derived factors are not sufficient to prevent hepatocellular atrophy in auxiliary rat liver transplantation models and that a potent hepatotrophic factor may exist in the venous drainage of the bowel distal to the duodenum.     

Methyl tert-butyl ether (MTBE) contamination in private wells near gasoline stations in upstate New York

BACKGROUND: Auxiliary liver transplantation has several advantages over standard orthotopic liver transplantation. However, functional competition has been reported even in auxiliary partial orthotopic liver transplantation (APOLT). We evaluated herein the interaction in APOLT between the native liver and the graft in terms of portal blood flow and regeneration. The need for diversion of the portal blood flow to the graft was also assessed. METHODS: A total of 15 patients received APOLT from living donors. Portal blood flow to the native liver was preserved in 6 patients, and the portal vein to the native liver was preemptively transected at the time of transplantation in 9 patients. RESULTS: Of the patients with preservation of the portal blood flow to the native liver, two showed inadequate graft portal blood flow just after operation, and in the other three patients the graft portal blood flow decreased or the graft atrophied after deterioration of the graft function. In the patients with preemptive transection of the portal vein to the native liver, optimal graft portal blood flow was obtained, and the native liver, supplied only by arterial inflow, supported a small-for-size graft until the graft regenerated. The damage to the native liver was minimal. CONCLUSIONS: Functional competition may occur in APOLT with preservation of the portal blood flow to the native liver, whereas preemptive transection of the native liver portal vein is a safe procedure and effectively prevents the portal steal phenomenon.     

Portal vein replacement by hepatic vein transposition

Successful reconstruction after portal vein resection in extended liver surgery has been performed by end-to-end anastomosis, patch, or graft interposition. Previously described techniques to obtain venous grafts for portal replacement necessarily have either an additional incision or an unsuitable diameter. We developed a new method of portal vein replacement using the excised hepatic vein. This technique can be applied in major liver resections for tumors infiltrating the portal vein that have a safe distance from the hepatic vein.     

Pulmonary fibrosis and lung cancer in the United States: analysis of the multiple cause of death mortality data, 1979 through 1991

BACKGROUND: Hepatocyte growth factor (HGF) plays a key role in the regulation of liver regeneration after hepatocyte damage. Changes in HGF production reflect the status of the regeneration process. METHODS: Serum concentrations of HGF and energy substrates were measured during and after liver transplantation in 30 recipients. RESULTS: In the patients with compromised grafts (group A) HGF concentrations were persistently high after reperfusion, whereas in the patients with well-functioning grafts (group B), HGF concentrations decreased rapidly and remained low 4 hours after reperfusion. The patients in group A who died had persistently high concentrations of HGF. The surviving patients with reversible primary graft dysfunction in group A exhibited low concentrations 48 hours after reperfusion. The decrease in HGF concentration preceded the decrease in aspartate aminotransferase concentration. The metabolic parameters that reflect carbohydrate metabolism by the graft paralleled the changes in HGF. CONCLUSIONS: HGF may be more sensitive and specific in predicting early graft function than prothrombin time, ratio, aspartate aminotransferase, or arterial ketone body ratio. The determination of HGF levels after liver transplantation may yield valuable information for evaluating early graft function and making an early decision to repeat a graft procedure in an acutely ill patient.     

Study of FHIT transcripts in normal and malignant breast tissue

The purpose of this study was to determine the utility of intraoperative Doppler ultrasound for the diagnosis and reduction of the vascular complications in liver transplantation. This study included 19 pediatric and 5 adult patients. In the pediatric group, 12 patients received living related liver transplantation (LRLT), two splitting liver transplantation (SLT), three reduced-size liver transplantation (RLT) and two full-size pediatric liver transplants (FPLT). The hemodynamics and waveform of the hepatic vein, portal vein and hepatic artery were evaluated by intraoperative Doppler ultrasound (US) after reperfusion of the graft. Unsatisfactory hemodynamics was identified in nine cases, including decrease hepatic venous flow (6-9 cm/s) with non-pulsative flat waveform (adults, n = 2 and LRLT, n = 2); portal vein thrombosis (LRLT, n = 1); decrease portal flow (8 mL/min/kg) (LRLT, n = 1); occlusion of the portal vein (SLT, n = 1); poor arterial flow with dampened artery waveform (FPLT, n = 2). These abnormalities were all successfully re-reconstructed by surgical procedures and achieved a graft survival rate of 100%. Two late vascular complications including hepatic venous thrombosis and recurrent portal vein stenosis with splenorenal shunt were discovered 1 month later. They were treated effectively by surgical thrombolectomy and percutaneous balloon dilatation and metallic coils embolization respectively. Three patients died of non-vascular complications and all patients who underwent LRLT survived with a resultant 87.5% overall survival rate. In conclusion, intraoperative Doppler US is efficient in detecting abnormal hepatic hemodynamics, which permits early intervention and hence a better prognosis for the patients. Re-reconstructive procedures were monitored closely under Doppler US guidance until proper flow and wave-form were established. This reduces post-transplant vascular complications and thereby eliminates the likelihood of a lethal complication that might call for re-transplantation.     

Donor hepatectomy for living-donor liver transplantation

Between September 1993 and November 1996, donor hepatectomy was performed in 22 living donor liver transplantation at Queen Mary Hospital, Hong Kong. In these donor operations, 7 extended right lobe grafts, 6 extended left lobe grafts and 9 left lateral segment grafts were obtained. The technique of donor operations consisted of initial hilar dissection, mobilization of the liver lobe, transection of the liver using ultrasonic dissector (without inflow or outflow vascular occlusion) at a plane on the left side of the middle hepatic vein for an extended right lobe graft, on the right side of the middle hepatic vein for an extended left lobe graft or on the right side of falciform ligament for a left lateral segment graft. The median blood loss was 775 ml. Complications occurred in 2 donors: one had incisional hernia and the other had biliary stricture. Both were treated successfully by re-operation. Currently all donors are well with completely normal liver biochemistry.     

Role of the donor liver in the origin of platelet disorders and hyperfibrinolysis in liver transplantation

We investigated the role of the donor liver in the origin of platelet disorders and hemostatic defects in liver transplantation. Eighteen pigs received an orthotopic or a heterotopic, auxiliary liver graft. Liver biopsies were taken for electron microscopic studies 5-10 min after reperfusion in nine animals. Blood samples were taken from the first hepatic outflow and from the systemic circulation before and 5 min after graft recirculation. Electron microscopy did not show any evidence of microthrombi or platelet aggregation in the graft, either after orthotopic liver transplantation or after heterotopic liver transplantation. Most blood platelets, which were lying free in the sinusoids, showed cell processes and many seemed to have lost their granulae, suggesting a degree of platelet activation. There were also signs of phagocytosis of platelets by the Kupffer cells. In the hepatic outflow, platelet count was significantly lower (p < 0.05) and fibrinolytic activity significantly higher (p < 0.01), than systemic post-reperfusion values. There were no important changes in the coagulation parameters. No significant changes were found between the effects on hemostasis of orthotopic and auxiliary graft reperfusion. In the second part of the study evidence for platelet activation was found after graft reperfusion in human liver transplantation. Plasma levels of platelet factor-4 and beta-thromboglobulin increased significantly after graft reperfusion. These studies suggest that platelet disorders and increased fibrinolytic activity are the major components of the hemostatic defect after graft recirculation in liver transplantation. Sequestration of platelets in the graft is probably due to the accumulation of (activated and degranulated) platelets in the sinusoids and phagocytosis by Kupffer cells.     

Prognostic value of malignant cells in pleural lavage at thoracotomy for bronchial carcinoma

BACKGROUND: It has been reported previously that liver grafts and liver cells seem to be tolerogenic, based on the high frequency of spontaneous tolerance after orthotopic liver transplantation in rodents and on the phenomenon of portal venous tolerance in other models. The purpose of the current study was to characterize in vivo immune responses to allogeneic hepatocytes transplanted into the portal circulation. METHODS: In this functional model of hepatocyte transplantation, "donor" hepatocytes from mice transgenic for human alpha1-antitrypsin (hA1AT) were transplanted by intrasplenic injection into host mice and the secreted hA1AT protein measured in host serum to determine hepatocellular graft survival. Host immune responses were assessed by measurement of donor-specific alloantibodies and delayed-type hypersensitivity responses. In some experiments, liver nonparenchymal cells (NPCs) were co-transplanted with the allogeneic hepatocyte transplant. RESULTS: Allogeneic hepatocyte transplant into immunocompetent hosts resulted in loss of host serum hA1AT by days 7-10 after transplant, whereas syngeneic hosts maintained long-term hepatocellular graft survival as reflected by persistence of serum hA1AT for > 20 weeks. Allogeneic hepatocyte transplantation resulted in the development of donor-specific alloantibody and delayed-type hypersensitivity responses, as well as a "second set" response of accelerated hepatocellular graft rejection after a second transplant. Pretransplantation or co-transplantation of donor-matched liver NPCs at the time of allogeneic hepatocyte transplantation did not prolong hepatocellular allograft survival. CONCLUSIONS: Allogeneic hepatocytes introduced into the portal circulation via intrasplenic injection are immunogenic not tolerogenic and stimulate a weak humoral and strong cell mediated host immune response in vivo. Co-transplantation or pretransplantation of allogeneic liver NPCs did not protect allogeneic hepatocytes from immunologic rejection.     

Portal vein ligation selectively lowers hepatic cytochrome P450 levels in rats

In rats, surgical creation of a portacaval shunt leads to hepatic atrophy and lowered levels of cytochrome P450, the key component of liver enzymes involved with drug metabolism. These effects are largely attributable to diversion of portal blood away from the liver and not to decreased hepatic blood flow. The present study has established a simpler model of portal blood diversion in order to examine the role of portal blood constituents in the regulation of hepatic cytochrome P450. Portal vein ligation was performed on male Wistar rats in which portasystemic anastomoses had been produced by subcutaneous transposition of the spleen. Portal vein ligation resulted in portal hypertension, as evidenced by splenomegaly, and in hepatic atrophy. In liver of rats with portal vein ligation, microsomal cytochrome P450 levels were significantly less than in sham-operated control rats, but cytochrome b5, NADPH-cytochrome c reductase, and glucose-6-phosphatase were unaltered. The activities of four mixed function oxidases also were reduced significantly in the liver of rats with portal vein ligation, the changes being greatest for ethylmorphine N-demethylase, a prototype substrate for the phenobarbital-inducible isoenzyme of cytochrome P450. In contrast, the activity of microsomal heme oxygenase, the rate-limiting step in catabolism of heme to bilirubin, was enhanced after portal vein ligation. Experiments in pair-fed rats showed that the changes observed in liver from rats with portal vein ligation could not be attributed to caloric deprivation. Administration of phenobarbital increased liver mass, cytochrome P450 levels, and mixed function oxidase activities both in rats with portal vein ligation and in controls, indicating that the liver of the ligated rats retained considerable protein synthetic capacity. It appears that hepatic atrophy and lowering of cytochrome P450 levels that follow portal vein ligation are consequences of altered exposure of the liver to factors normally present in portal blood, and that the same alterations may also enhance heme oxygenase activity.     

Replacement of the retrohepatic vena cava in segmental liver transplantation

Reduced grafts represent an important technical development in paediatric liver transplantation. The use of a left lateral segment graft has required preservation of the native inferior vena cava to "piggy-back" the graft onto it. We report four children who underwent left lateral segment transplantation with caval replacement using the donor iliac vein because the native retrohepatic inferior vena cava was small, friable or difficult to preserve. There were no caval or hepatic vein complications post-transplant and the donor iliac vein proved to be a satisfactory interpositional graft. The technique offers the advantages of a wider retrohepatic cava avoiding venous outflow or caval obstruction, provides good tissue to suture and is well suited for the triangulation technique of the left hepatic vein.     

The middle colic vein: an alternative source of portal inflow in orthotopic liver transplantation complicated by portal vein thrombosis

BACKGROUND: Portal vein thrombosis (PVT) was previously considered a contraindication to orthotopic liver transplantation (OLT) since adequate portal blood supply is mandatory for graft function and patient survival. Improvements in surgical technique, however, have meant that this problem now can be circumvented in most instances. Nevertheless portal vein thrombosis remains an obstacle in OLT and is associated with increased incidence of primary non-function and long-term liver failure. METHODS: A 55-yr-old patient underwent OLT for secondary biliary cirrhosis associated with hepatitis C infection and complicated by long standing PVT. Involvement of the portal, mesenteric, and splenic veins prevented standard portal venous reconstruction. Portal inflow was accomplished by a side-to-end anastomosis between the middle colic vein and the donor portal vein. RESULTS: Hepatic reperfusion and subsequent liver function were excellent. Portal blood flow, as measured by color-enhanced Doppler ultrasound, was normal following surgery until discharge. The post-operative course was complicated by abdominal wound dehiscence and recurrent cytomegalovirus (CMV) infection. The patient was discharged in good clinical condition, with excellent liver function and patent portal vein 89 d after OLT. CONCLUSIONS: The middle colic vein is a novel, not previously described, source of portal venous inflow for OLT complicated by extensive splanchnic venous inflow thrombosis.     

Liver as a focus of impaired oxygenation and cytokine production in a porcine model of endotoxicosis

OBJECTIVES: To determine whether the liver is a focus of insufficient oxygenation and whether liver is a source of tumor necrosis factor (TNF) and interleukin-6 (IL-6) in a porcine model of endotoxicosis. DESIGN: In vivo, prospective, controlled, repeated-measures, experimental study. SETTING: Experimental physiology laboratory in a university. SUBJECTS: Juvenile pigs, weighing 22 to 35 kg. INTERVENTIONS: Catheters for blood sampling were inserted into the carotid artery, portal vein, hepatic vein, and pulmonary artery of anesthetized animals. Ultrasonic flow probes were placed on the portal vein and the hepatic artery. During surgery, normal saline was infused intravenously at 25 mL/kg/hr. Following stabilization, animals were allocated randomly to one of two groups. The endotoxemic group (n = 6) received 50 mg/kg of purified Escherichia coli lipopolysaccharide infused into the external jugular vein over 1 hr. The control group (n = 6) received a sham saline infusion infused over 1 hr. Once the endotoxin or sham infusion was initiated, the rate of the intravenous saline infusion was increased to 48 mL/kg/hr for the remainder of the experiment. Measurements were obtained before the endotoxin or sham infusion, immediately after the infusion, and every 30 mins thereafter for 4 hrs. MEASUREMENTS AND MAIN RESULTS: Blood gases, lactate, and bioactive TNF and IL-6 concentrations were measured from the carotid artery, portal vein, hepatic vein, and pulmonary artery. The porcine model is characterized by systemic hypotension, pulmonary hypertension, and maintenance of cardiac output. Despite decreased hepatic oxygen delivery in endotoxemic animals (p < .02), there was no change in hepatic oxygen consumption compared with controls. Throughout the experiment, there was net hepatic consumption of lactate in both groups. There was no significant hepatic production (or consumption) of TNF or IL-6 in either group. CONCLUSIONS: In this porcine model of endotoxicosis, there is a reduction of hepatic oxygen delivery but dysoxia is not present. The liver is not a source of TNF or IL-6 in this model of endotoxicosis.     

Repairing bone defect with autogenous periosteal pieces in coagulum: experimental study and clinical application

Sixty patients who received 75 consecutive liver grafts and had routine Doppler sonography monitoring in the early postoperative period (three times a day) were reviewed for vascular complications. Thrombosis of the hepatic artery was detected in seven patients (3, 4, 20, 24, 48, 70 and 84 h after liver transplantation) and was then confirmed by emergency laparotomy in six cases. In one patient, thrombosis was verified by angiography before laparotomy. In two patients thrombectomy was successful, in five patients retransplantation had to be performed. Portal vein occlusion was detected in three patients (24, 26 and 90 h after transplantation) and all were successfully treated by thrombectomy and partial arterialization of the portal vein. Colour Doppler sonography was associated with no false-positive or -negative results. The specificity was 100% for the diagnosis of hepatic artery and portal vein thrombosis. In our opinion colour Doppler sonography will be able to replace time-consuming angiography in vascular diagnostics in the early postoperative phase after liver transplantation. Furthermore, there is evidence that frequent use of this non-invasive technique permits early detection of clinically unsuspected vascular complications and subsequent immediate relaparotomy, which is linked to a reduction in the rate of retransplantation.     

Improved results of liver transplantation in patients with portal vein thrombosis

OBJECTIVE: To analyze the impact of preexisting portal vein thrombosis (PVT) on the operative management and outcome of liver transplantation. DESIGN: Retrospective review of 1423 patients who received transplants over 11 years. SETTING: Tertiary referral center. PATIENTS OR OTHER PARTICIPANTS: Seventy patients who underwent liver transplantation who had preexisting PVT. INTERVENTIONS: Portal vein thromboendovenectomy, vein grafting, or use of portal collateral veins for inflow during liver transplantation. MAIN OUTCOME MEASURES: Postoperative PVT, intraoperative transfusion, retransplantation rate, 30-day and 1-year actuarial survival rates. RESULTS: Operative management consisted of thromboendovenectomy in 61 cases, vein graft to the superior mesenteric vein in 6 cases, and vein graft to other mesenteric veins in 3 cases. The incidence of posttransplant PVT was 3% (n = 2). The mean +/- SD transfusion requirement was 23 +/- 18 U. The 1-year actuarial survival rate was 74% but improved from 66% in the first 35 cases to 82% in the latter 35 cases. CONCLUSIONS: Thromboendovenectomy is the procedure of choice for PVT. Results of liver transplantation in patients with PVT improve significantly with experience gained and are equivalent to results in patients without PVT.     

Testosterone concentrations, testes weight and morphology of mule drakes (Muscovy drake x Khaki Campbell)

BACKGROUND: Transjugular intrahepatic portosystemic shunts (TIPS) are sometimes used to reduce the risk of variceal bleeding or treat intractable ascites before orthotopic liver transplantation (OLT). TIPS usually do not make OLT more difficult, but rarely, malposition of TIPS can significantly complicate OLT. METHOD and RESULTS: The following report describes a patient in whom an initially well-placed Wallstent migrated to the confluence of the splenic and superior mesenteric veins. During liver transplantation, the portal vein containing the Wallstent was completely resected, and the portal vein was reconstructed with donor iliac vein. After sewing the iliac vein onto the portal remnant, the liver transplant was completed under portosystemic bypass. The patient had an uneventful recovery. CONCLUSIONS: Wallstents can migrate within the portal vein. An interposition graft of donor vein allows full resection of the portal vein containing a migrated stent and facilitates portosystemic bypass and portal anastomosis.     

Anti-GBM glomerulonephritis in mice lacking nitric oxide synthase type 2

To determine the relationship between quantitative Doppler parameters of portal, hepatic, and splanchnic circulation and hepatic venous pressure gradient (HVPG), variceal size, and Child-Pugh class in patients with alcoholic cirrhosis, we studied forty patients with proved alcoholic cirrhosis who underwent Doppler ultrasonography, hepatic vein catheterization, and esophagoscopy. The following Doppler parameters were recorded: time-averaged mean blood velocity, volume flow of the main portal vein flow, and resistance index (RI) of the hepatic and of the superior mesenteric artery. Doppler findings were compared with HVPG, presence and size of esophageal varices, and Child-Pugh class. There was a significant inverse correlation between portal velocity and HVPG (r = -.69), as well as between portal vein flow and HVPG (r = -.58). No correlation was found between RI in the hepatic artery or superior mesenteric artery and HVPG. No correlation was found between portal vein measurements and presence and size of varices. Severe liver failure was associated with lower portal velocity and flow. In patients with alcoholic cirrhosis, only portal vein blood velocity and flow, but neither hepatic nor mesenteric artery RI, are correlated to the severity of portal hypertension and to the severity of liver failure.     

Vascular reconstruction using left renal vein graft in advanced hepatobiliary malignancy

BACKGROUND/AIMS: In surgical resection for advanced hepatobiliary malignancies involving the portal vein and inferior vena cava, vascular reconstruction is usually required. We utilized left renal vein grafts for vascular reconstruction in cases of these malignancies, and their clinical significance is evaluated in this study. METHODOLOGY: Left renal vein grafts were utilized for reconstruction of the portal vein in four patients and patch repair of the inferior vena cava was performed in two patients with advanced hepatobiliary malignancies. All six patients underwent hepatic resection with vascular resection and reconstruction. Postoperative renal function and graft patency were assessed. RESULTS: Transient slight renal disturbances appeared in some patients, but there was no severe renal dysfunction requiring specific therapy. Graft patency was maintained during the follow-up period in all patients. CONCLUSION: The use of left renal vein grafts as autovein grafts seems appropriate in cases involving reconstruction of the portal vein and in those involving patch repair of the inferior vena cava defect in surgical resection for advanced hepatobiliary malignancies.     

Can clamping of splenic vessels prevent abrupt increase of portal vein pressure and migration of transplanted hepatocytes to the liver after intrasplenic hepatocyte transplantation?

BACKGROUND/AIMS: It is well known that hepatocyte transplantation can retain some proper functions, significantly improve the survival rate of rats with different models of acute fulminant hepatic failure, correct some congenital genetic disorders, and improve liver function in cirrhosis. Portal hypertension and hepatic embolization have been described following intrasplenic hepatocyte transplantation. We evaluated the effect of temporary occlusion of splenic vessels on changes in portal vein pressure and on distribution of transplanted hepatocytes after hepatocyte transplantation into the spleen in normal rats. METHODOLOGY: Liver cirrhosis has been induced in rats by 1% dimethylnitrosamine (Sigma, St. Louis, Mo) dissolved in normal saline at the dose of 10 ml of DMN/Kg, i.p., 3 consecutive days a week for 4 weeks. Donor hepatocytes were harvested by in situ ethylenediaminetetraacetic acid (EDTA) perfusion. Changes in portal vein pressures were monitored by a pressure monitor and distribution of transplanted hepatocytes was assayed by measurement of radioactivity of 51Cr-labeled transplanted hepatocytes according to clamping or non-clamping during intrasplenic hepatocyte transplantation. RESULTS: The changes in portal pressure remained significantly high 10 min after hepatocyte transplantation in the nonocclusion groups compared to the occlusion groups. However, the changes in portal vein pressures in cirrhotic rats returned to normal faster than in normal rats after cell transplantation in the nonocclusion groups. The distribution of 51Cr-labeled transplanted hepatocytes into the spleen significantly diminished radioactivity of the liver at 10 min, 2 hours, and 24 hours in the occlusion groups compared to the nonocclusion groups. Also, duration of clamping time of splenic vessels did not influence the initial distribution of transplanted hepatocytes at the time of intrasplenic hepatocyte injection. CONCLUSIONS: These results suggested that temporary occlusion of splenic vessels should be routinely used during intrasplenic hepatocyte transplantation.     

Analysis of postoperative liver function of donors in living-related liver transplantation: comparison of the type of donor hepatectomy

BACKGROUND: There is a potentially significant risk to the donor in living-related liver transplantation. METHODS: We analyzed surgical risk and stress to 35 donors in living-related liver transplantation with special reference to the types of donor hepatectomy. Donor surgery was performed in one of three ways: (1) lateral segmentectomy without ligation of the middle hepatic vein (MHV) in the remnant liver (group 1, n=21); (2) lateral segmentectomy with ligation of MHV in the remnant liver (group 2, n=6); and (3) left lobectomy with MHV (group 3, n=8). RESULTS: No critical complications were observed in any group. The postoperative enzyme levels in group 2 were significantly higher than those in groups 1 and 3 (P<0.01). Although blood loss was covered by autologous blood transfusion in the first six cases, no banked blood was transfused in any of the cases. Surgical duration was significantly longer and blood loss was significantly greater in group 3 than in group 1 (P<0.05). Follow-up computed tomography showed atrophic changes in segment IV in groups 1 and 2. No remarkable changes were seen in segments V or VIII in any of the three groups. CONCLUSION: Regardless of the donor hepatectomy procedure, serious complications did nor occur after surgery. Although it should be noted that the type of donor hepatectomy affects postoperative donor liver function, left lateral segmentectomy with ligation of MHV in the remnant liver is a useful method for obtaining liver grafts from living-related donors who have unusual anatomic variations of the hepatic veins.     

Effects of low molecular weight heparin, alone or combined with antithrombin III, on mortality, fibrin deposits and hemostatic parameters in endotoxin-induced disseminated intravascular coagulation in rabbits

Percutaneous transhepatic portal vein embolization (PTPE) has been used to decrease the risk of hepatic failure after hepatectomy in patients with poor liver function. The effect of PTPE on hepatic drug-metabolizing activities is not clear. Therefore we examined the effect of portal vein branch ligation, a model of PTPE, on hepatic drug-metabolizing activities in Sprague-Dawley rats. Ligated and nonligated lobes were harvested separately. Drug-metabolizing activities and concentrations of components of the microsomal cytochrome P-450 monooxygenase system were examined. In ligated lobes, drug-metabolizing activities (lidocaine and aminopyrine) and enzymatic concentrations of the microsomal cytochrome P-450 monooxygenase system gradually decreased over 10 days. In nonligated lobes these functions were depressed rapidly to 60% of those before PBL but then recovered 10 days after PBL. From the viewpoint of drug metabolism, hepatic dysfunction occurred in both ligated and nonligated lobes.