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PubMed2006

Transhepatic lactate gradient in relation to liver ischemia/reperfusion injury during major hepatectomies.

Hepatectomies performed under selective hepatic vascular exclusion are associated with a series of events culminating in ischemia/reperfusion injury, a state that shares common characteristics with situations known to result in global or regional hyperlactatemia. Accordingly, we sought to determine whether lactate is released by the liver during hepatic resections performed under blood flow deprivation and what relation this has to a possible systemic hyperlactatemic state. After ethical approval, 14 consecutive patients with resectable liver tumors subjected to hepatectomy under inflow and outflow occlusion of the liver were studied. Lactate concentrations were assessed in simultaneously drawn arterial, portal venous, and hepatic venous blood before liver dissection and 50 minutes postreperfusion. Moreover, the transhepatic lactate gradient (hepatic vein - portal vein) was calculated to see if there was net production or consumption of lactate. Before hepatic dissection, the transhepatic lactate gradient was negative, suggesting consumption by the liver. Fifty minutes after reperfusion, this gradient became significantly positive, demonstrating release of lactate by the liver (0.12 +/- 0.31 vs. -0.38 +/- 0.30 mmol/L, P < 0.05). The magnitude of lactate release correlated with systemic arterial lactate levels at the same time point (r(2) = 0.63, P < 0.001). A weaker but significant correlation was demonstrated between the transhepatic lactate gradient postreperfusion and systemic arterial lactate levels 24 hours postoperatively (r(2) = 0.41, P = 0.013). A strong correlation between the transhepatic lactate gradient postreperfusion and peak postoperative aspartate aminotransferase values was also demonstrated (r(2) = 0.73, P < 0.001). The liver becomes a net producer of lactate in hepatectomies performed under blood flow deprivation. This lactate release can explain some of the systemic hyperlactatemia seen in this context and relates to the extent of ischemia/reperfusion injury.

Aged↗

PubMed1989

Expression of c-raf-1 and A-raf-1 during regeneration of rat liver following surgical partial hepatectomy.

The major objective of this study was to investigate the expression of members of the raf family of proto-oncogenes during rat liver regeneration. The steady-state level of expression of both c-raf-1 and A-raf-1 increased three- to fivefold 18-24 h following partial hepatectomy, and it returned to basal levels by 72 h. Expression of c-myc and Ha-ras mRNA was increased at 3 and 18-24 h, respectively, confirming previous reports. Increased steady-state levels of c-raf-1, A-raf-1, and Ha-ras mRNA were also detected in hepatocytes isolated from rat liver 24 h after partial hepatectomy. Thus, elevated expression of the raf genes closely correlated with that of Ha-ras, beginning at 12 h and reaching maximal levels during the first peak of DNA synthesis following partial hepatectomy.

Animals↗

PubMed2005

Partial hepatectomy induced liver proteome changes in mice.

Acceleration of liver regeneration could be of great clinical benefit in various liver-associated diseases. However, at present little is known about therapeutic interventions to enhance this regenerative process. Our limited understanding and the complexity of the mechanisms involved have prevented the identification of new targets for treatment. Here we propose a broad-range proteomic approach to this problem that makes possible the simultaneous study of different signaling and metabolic pathways on the liver proteome. Changes in protein expression in mouse livers (n = 5 per group) at 6 h and 12 h after partial hepatectomy and sham operation, as compared to untreated controls, were analyzed using two-dimensional gel electrophoresis, mass spectrometry (MS), and mass fingerprinting. Twelve proteins, identified by MS, were up-regulated by at least 2-fold after partial hepatectomy. These included adipose differentiation-related protein, gamma-actin, enoyl coenzyme A hydratase 1, serum amyloid A and eukaryotic translation initiation factor 3. These results indicate that liver regeneration following partial hepatectomy affects various signaling and metabolic pathways.

Animals↗

PubMed1996

Proteoglycan gene expression in rat liver after partial hepatectomy.

Liver regeneration is regulated by several factors. Among these extracellular matrix plays a crucial role in the restoration of normal structure. Proteoglycans are major components of extracellular matrix and they are able to bind growth factors implicated in liver growth. We studied syndecan, perlecan, fibroglycan, and decorin expression after partial hepatectomy in rats by Northern blot analysis. A strong early upregulation was observed at 30 min in decorin expression which was followed by the first syndecan and perlecan peaks at 2 and 4 hours after hepatectomy. At 24 hours, which is the peak of hepatocyte DNA synthesis, all these three proteoglycans had elevated steady state transcript level. Fibroglycan message decreased after partial hepatectomy and remained low during the experimental period. The different expression pattern of the proteoglycans suggests that these extracellular matrix components may selectively influence the regeneration process.

Animals↗

PubMed1997

Inhibition of tumor necrosis factor-alpha production retards liver regeneration after partial hepatectomy in rats.

We studied the effects of a tumor necrosis factor-alpha (TNF-alpha) production inhibitor E3330, [(2E)-3-[5-(2,3-dimethoxy-6-methyl-1,4-benzoquinolyl)]-2-nonyl-2-+ ++propenoic acid] on liver regeneration in rats subjected to 70% partial hepatectomy. The BrdU labeling index was 53.5 +/- 3.8% 24 h after partial hepatectomy alone and was significantly inhibited by E3330 (25 and 50 mg/ kg) in a dose-dependent manner (43.3 +/- 2.1% and 19.0 +/- 10.3%, respectively; p < 0.05, p < 0.01). In these 3 groups, TNF-alpha protein levels in liver tissue were 187 +/- 18, 123 +/- 47, and 89 +/- 33 pg/mg total protein, respectively, with a significant decrease by E3330 administration (p < 0.01). TNF-alpha mRNA expression in liver tissue was also reduced by E3330. These results suggest that TNF-alpha promotes liver regeneration after partial hepatectomy.

Alanine Transaminase↗

PubMed1997

Transient down-regulation of inhibin-betaC expression following partial hepatectomy.

Inhibin-betaC is a recently described TGF-beta family member most homologous to inhibin-betaA and inhibin-betaB. By Northern analysis, inhibin-betaC mRNA was detected exclusively in the liver among a large number of adult mouse tissues surveyed. The expression of inhibin-betaC mRNA in adult liver dropped sharply and transiently following partial hepatectomy. At 6 and 12 hours following partial hepatectomy, the levels of inhibin-betaC mRNA were at least 8-fold lower than in control animals. The liver specificity of inhibin-betaC expression and its down-regulation following partial hepatectomy suggest that inhibin-betaC may function as a negative regulator of liver growth.

Animals↗

PubMed2001

Lower activity of CCAAT/enhancer-binding protein and expression of cyclin E, but not cyclin D1, activating protein-1 and p21(WAF1), after partial hepatectomy in obstructive jaundice.

CCAAT/enhancer-binding protein (C/EBP)-alpha stabilizes p21(WAF1), whereas activating protein-1 (AP-1) and C/EBP-beta enhance cyclin D1 and cyclin E expression, respectively, during the progress of liver regeneration. In this study, we investigated the differences in the transcription factors and cell cycle regulators between obstructive jaundiced and control rats before and after hepatectomy accompanied with a release of biliary obstruction by internal biliary drainage. The expressions and activities of C/EBP-alpha and -beta were significantly decreased in the jaundiced group concomitant with the significantly lower cyclin E expression after hepatectomy than in the controls. The activities of AP-1, cyclin D1 and p21(WAF1) were not significantly different between the two groups. These results suggest that obstructive jaundice inhibits hepatic expression and activity of C/EBP, resulting in the impaired cyclin E expression that is partly responsible for the cell cycle dysfunction after hepatectomy.

Animals↗

PubMed2002

Inhibited activities in CCAAT/enhancer-binding protein, activating protein-1 and cyclins after hepatectomy in rats with thioacetamide-induced liver cirrhosis.

Transcriptional activation of nuclear factor (NF)-kappaB, signal transducers and activators of transcription (STAT) 3, activating protein (AP)-1 and CCAAT/enhancer-binding protein (C/EBP) plays an important role in liver regeneration by modulating cell cycle regulators. The regeneration of cirrhotic liver after hepatectomy is inhibited despite intact expression of growth factors. To elucidate the mechanism involved, regeneration responses in growth factor receptors, transcription factors, and cell cycle regulators after two-thirds hepatectomy were compared between rats with thioacetamide-induced cirrhotic and normal liver. The expression of c-met and epidermal growth factor receptor analyzed by RT-PCR and immunohistochemistry did not differ between the two groups. The activities of C/EBP and AP-1 evaluated by electrophoretic mobility shift assay were significantly inhibited in the cirrhotic group compared with those in the control group, but not those of NF-kappaB and STAT3. The expression of cyclin-D1, -E, and -A assessed by Western blot analysis was significantly decreased in the cirrhotic group compared with the control group. The level in p21(Cip1) or p27(Kip1) did not differ between the two groups. The liver regeneration estimated by the rates of [(3)H]thymidine incorporation into DNA and staining of proliferating cell nuclear antigen was significantly lower in the cirrhotic rats than in the controls. In conclusion, downregulation of cyclin -D1, -E, and -A expression, which may be induced by impaired activities of C/EBP and AP-1, is responsible for the decreased regenerative capacity of cirrhotic liver after partial hepatectomy.

Animals↗

PubMed1993

Differential patterns of expression of three C/EBP isoforms, HNF-1, and HNF-4 after partial hepatectomy in rats.

Regenerating liver provides a system for studying the mechanisms controlling regulated proliferation of differentiated hepatocytes. A set of transcription factors termed hepatocyte nuclear factors (HNF-1, -3, -4) and CCAAT/enhancer binding protein (C/EBP) isoforms are known to regulate several genes predominantly expressed in the liver. To assess whether these factors might be involved in the hepatocyte proliferation program, we have studied the expression of the three C/EBP isoforms C/EBP alpha, C/EBP beta, and C/EBP delta and the two hepatocyte-enriched transcription factors, HNF-1 and HNF-4, in rat liver at various time points after partial hepatectomy and sham operations using transcriptional "run-on" assays and Northern blot and Western blot experiments. We report here that partial hepatectomy in rats leads to dramatic changes in the pattern of expression of some of these genes. The three C/EBP isoforms are differentially regulated in response to partial hepatectomy and are likely to play different roles in determining the proliferation/differentiation state of hepatocytes. In particular, C/EBP alpha expression is rapidly down-regulated, whereas C/EBP delta is induced. C/EBP beta expression is also increased, although an increase is also observed after sham operation. The drastic decrease in C/EBP alpha under these conditions of active DNA synthesis and rapid cell proliferation further supports the concept of a potential incompatibility between high C/EBP alpha protein levels and cell proliferation. The patterns of transcriptional rates of HNF-1 and HNF-4 during the different stages of the regenerative process are similar. However, HNF-1 steady-state mRNA and protein levels are significantly changed while HNF-4 remains virtually unaffected, indicating that post-transcriptional mechanisms are also involved in the regulation of HNF-1 gene expression.

Animals↗

PubMed1995

Alterations of lipid contents in blood, hepatocytes, and enterocytes in the early stage of acute liver failure induced by 90% hepatectomy in the rat.

Potential alterations in lipid metabolism in the early stage of acute liver failure are poorly elucidated. In the present study, acute liver failure was induced by subtotal hepatectomy (90%) in the rat in order to investigate early alterations in lipid contents in blood, hepatocytes, and enterocytes. Hypocholesterolemia and hypotriglyceridemia appeared 2 and 6 hr following subtotal hepatectomy. Plasma levels of high density lipoprotein-cholesterol were significantly lower in rats with acute liver failure than in controls, which may be associated with hypocholesterolemia. An increase in erythrocyte phospholipids and triglycerides was seen from 2 hr on after hepatectomy. The content of phospholipids and triglycerides was reduced in isolated enterocytes from the proximal small intestine and increased in enterocytes from the distal small intestine. Isolated hepatocytes from the remnant liver exhibited an increase in phosphatidylethanolamine and a decrease in phosphatidylinositol. Levels of enterocyte phosphatidylserine were elevated in both the proximal and the distal small intestine, while they diminished in the distal small intestine. Sphingomyelin content increased in the proximal small intestine. The recognition of lipid alterations in the intestine-liver-systemic circulation axis in the early stage of acute liver failure may be beneficial in improving the recovery from acute liver failure.

Animals↗

PubMed1998

The Kidney's role in glucose balance following partial hepatectomy.

It has long been believed that the liver is the major contributor to glucose balance during fasting and stressful situations. Recently, investigators have implicated the kidney as having a significant contribution to systemic glucose appearance. We studied the relative contributions of the kidney and liver to glucose homeostasis in fasted nonoperated, sham-operated, and 70% hepatectomized rats. Systemic glucose appearance, renal glucose release and uptake, and hepatic glucose release were determined by glucose balance and isotopic dilution techniques. Systemic glucose appearance remained unchanged following hepatectomy. There was a significant output of glucose by the kidney in all groups, accounting for >50% of total glucose appearance. Despite the kidney's appreciable contribution to circulating glucose in the postabsorptive state, renal glucose release was not increased in the hepatectomized rats compared to controls. Total glucose appearance was maintained following hepatectomy by an increase in hepatic glucogenesis. There was a significant increase in the rate of hepatic glucose release from resected rats when normalized to gram of remaining liver (P < 0.001). Despite the substantial amount of renal glucose output in the postabsorptive state, preservation of glucose balance following 70% hepatectomy is accomplished by adaptation in hepatic glucose output.

Animals↗

PubMed2000

c-Jun does not mediate hepatocyte apoptosis following NFkappaB inhibition and partial hepatectomy.

Inhibition of the transcription factor nuclear factor kappa B (NFkappaB) induces marked hepatocyte apoptosis and liver dysfunction after partial hepatectomy (PH) in rats. Hepatocyte apoptosis may be due to direct inhibition of NFkappaB-induced hepatocyte survival genes or due to indirect increased signaling through the stress-activated protein kinase pathway (SAPK), resulting in increased c-Jun. c-Jun, an AP-1 transcription factor, induces apoptosis in fibroblasts. Our aim was to determine if hepatocyte apoptosis following inhibition of NFkappaB and partial hepatectomy in rats is due to increased c-Jun. Adult male Sprague-Dawley rats (200 g) were injected intraportally with 6 x 10(9) PFU adenoviral vector containing luciferase (Ad5Luc) or superrepressor IkappaB (Ad5IkappaB) transgene that inhibits NFkappaB translocation into the nucleus. Two-thirds PH was performed 24 h after vector administration, and the remnant liver was harvested 30 min or 24 h after PH. Northern and Western blots were performed to examine the presence of IkappaB and c-Jun. A GST c-Jun kinase assay was used to examine Jun-N-terminal kinase (JNK) activity. AP-1 DNA binding activity was assessed by electrophoretic mobility shift assay. TUNEL assay was performed to assess apoptosis. All rats receiving adenoviral vectors expressed the luciferase or superrepressor IkappaB transgenes. c-Jun mRNA, protein levels, and DNA binding activity were not increased in rats treated with Ad5IkappaB at 30 min after PH compared to rats injected with Ad5Luc. Jun kinase activity increased following partial hepatectomy, but activity was similar in Ad5Luc- and Ad5IkappaB-treated animals. AP-1 DNA binding activity was not altered substantially in rats treated with Ad5IkappaB. The percentage of apoptotic hepatocytes was similar between Ad5Luc- and Ad5IkappaB-injected animals at 0 h, but livers from Ad5IkappaB-treated rats had increased apoptosis at 24 h compared to Ad5Luc rats (24% vs. 4%) after PH. Hepatocyte apoptosis after NFkappaB inhibition and PH is not mediated by increased JNK activity or c-Jun.

Adenoviridae↗

PubMed1977

Effect of partial hepatectomy on the interrenal tissues of Xenopus laevis (Daudin).

Partial hepatectomy was carried out on Xenopus laevis to investigate its influence on the endocrine system. In addition to other endocrine effects, a marked hypertrophy and stimulation of the interrenal gland was observed. Activated cells contain mitochondria with extended and irregularly coiled tubules embedded in a low electron dense matrix. Hepatectomy induces two phases of proliferation [3 and 35 days postoperative (p.o.)]. After 106 days p.o. giant mitochondria possessing narrow and closely packed, parallel tubules surrounded by an electron dense matrix indicate a phase of inactivation. The smooth endoplasmic reticulum and the Golgi apparatus proliferate after hepatectomy. During activation the high lipid content seen in controls in decreased significantly.

Adrenal Glands↗

PubMedDate not supplied

Impaired liver function and long-term prognosis after hepatectomy for hepatocellular carcinoma.

Patients with hepatocellular carcinoma (HCC) show a wide variety of histologic changes in the noncancerous liver parenchyma, and these changes may affect the prognosis. In this study, we grouped patients according to the extent of liver impairment and investigated their long-term prognosis after hepatectomy for HCC. A total of 194 patients were divided into two groups according to their plasma clearance rate of indocyanine green (ICG-K) values: those with values < 0.13 min-1 (group A, n = 97) and those with values of > or = 0.13 min-1 (group B, n = 97). Eighty-nine patients with stage I or II HCC were also divided into two groups: those with values < 0.13 min-1 (group C, n = 52) and those with values of > or = 0.13 min-1 (group D, n = 37). Group B patients tended to survive longer than group A patients during 4 years after hepatectomy, and group D patients survived significantly longer than group C patients (p < 0.01). There was no significant difference in the recurrence-free survival rates between those in groups A and B or groups C and D. Because patients with poor liver function frequently had multiple recurrent lesions and limited therapeutic options, patients with good liver function received more intensive treatment. In conclusion, the extent of liver impairment is one of the factors determining long-term prognosis after hepatectomy for HCC, especially during the early stage of the disease.

Adult↗

PubMed1996

Changes in liver blood flow after hepatectomy in conscious dogs.

Hepatic circulation after hepatectomy was investigated in conscious dogs under fasting and feeding conditions. After a 40% hepatectomy, both the hepatic arterial and portal blood flow were measured simultaneously using ultrasonic transit time flowmeters. During fasting, the total hepatic blood flow (i.e., the sum of arterial and portal blood flow) changed in a biphasic pattern after hepatectomy. The first peak (517.9 +/- 42.7 ml/min; 130.1% of preoperative flow) was seen on the 1st postoperative day (POD) and the second peak (444.8 +/- 25.6 ml/min; 112.7% of preoperative flow) occurred on the 7th POD. The portal flow demonstrated the same biphasic changes as the total hepatic flow, although the hepatic arterial flow showed only the first peak. A heart rate analysis suggested that the first peak was probably due to hyperdynamic circulatory conditions, as has been previously reported. In addition, the existence of the second peak was established by the present study. The postprandial hepatic blood flow decreased during the first 2 weeks postoperatively, but exceeded the presurgical levels on PODs 21 and 28.

Animals↗

PubMed1994

Facilitation of liver regeneration after partial hepatectomy by ventromedial hypothalamic lesions in rats.

Whether or not the hypothalamus is involved in initiating hepatic DNA synthesis after partial hepatectomy is unclear. To determine the role of the ventromedial hypothalamic nuclei in liver regeneration after partial hepatectomy, we studied hepatic DNA synthesis during liver regeneration in rats with bilateral lesions of these nuclei. Lesions of the ventromedial hypothalamus accelerated the increase in hepatic DNA synthesis and raised the peak level of thymidine incorporation after partial hepatectomy. These effects of hypothalamic lesions were completely inhibited by hepatic vagotomy. Thus, lesions of the ventromedial hypothalamus appear to promote hepatic regeneration by increasing vagal stimulation of the liver.

Animals↗

PubMed1994

Regulating factors of liver regeneration after hepatectomy.

The factors regulating liver regeneration were studied by measuring changes in the liver volume and serum hepatocyte growth factor (HGF) levels after hepatectomy. Changes in the liver volumes were studied in 68 hepatectomized patients, including (A) hepatoma patients who had chronic hepatitis or liver cirrhosis (n = 44) and (B) metastatic liver cancer patients who had normal liver parenchyma (n = 24). The hepatic volume increased by 13.8% of the remnant hepatic volume in group A and by 49.1% in group B. The examined factors included the percentage of resected liver volume (%RLV) and the results of laboratory tests. Regression analysis showed that in group A, both %RLV (beta = 0.46) and the serum total bilirubin (T-Bil) level (beta = -0.33) correlated significantly with the extent of liver regeneration and that in group B, only %RLV (beta = 0.78) correlated significantly with the regeneration. Serum HGF levels after hepatectomy were studied in 21 hepatectomized patients, including 11 hepatoma patients and 10 patients with some types of metastatic liver cancer. Serum HGF levels increased significantly after surgery in all 21 patients. Regression analysis, however, showed that the change in HGF was related to liver cirrhosis (beta = 0.46) and to the maximal postoperative T-Bil level (beta = 0.51) but not to the extent of liver regeneration after hepatectomy. These results suggest that liver regeneration is regulated primarily by factors relating to the percentage of the resected liver parenchyma and that serum HGF levels do not directly relate to liver regeneration after surgery.

Aged↗

PubMed1997

A nonspecific colonic ulcer occurring after hepatectomy: report of a case.

We herein report the case of a 53-year-old man with a nonspecific acute colonic ulcer whose liver function deteriorated after he had undergone hepatectomy. He was referred to our hospital for a hepatoma caused by hepatitis B virus and a right hemihepatectomy was performed. His liver function was poor after the operation, and minor complications such as pleural effusion and biliary fistula developed. A large amount of melena was seen 29 days after the hepatectomy and he developed hemorrhagic shock. Superior mesenteric arteriography revealed pooling of blood in both the hepatic flexure of the ascending colon and the cecum. An emergency right hemicolectomy was performed. There was a 5 x 1-mm ulcer 18 cm distal to the ileocecal valve. Numerous erosions were observed to be scattered throughout the colonic mucosa. The patient recovered slowly and was discharged 6 months after the hepatectomy. This is the first report of an acute colonic ulcer that could have been caused by liver dysfunction.

Carcinoma, Hepatocellular↗