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PubMed1996

Anatomical hepatectomy for resection or transplantation.

BACKGROUND: Anatomical resection has become the basis for the treatment of hepatic tumors recognizing the portal-based intrahepatic architecture of the liver. In transplantation, these principles have been applied to the creation of partial liver grafts used to treat pediatric recipients with grafts from adult donors. In this study we reviewed the results of application of these techniques in 60 patients undergoing major hepatectomy and in 47 liver transplants in children. METHODS: Records of patients undergoing resection and children undergoing transplantation were reviewed. A descriptive study was performed characterizing the methods and results achieved using anatomic hepatectomy. Outcomes analyzed included surgical morbidity and survival. RESULTS: Sixty consecutive patients underwent major hepatectomy without operative mortality (60 days). Complications occurred in 26% of patients, requiring reoperation in 2 cases (3%); median hospital stay was 8.5 days. Of 47 liver transplants in children, 57% utilized partial grafts, and living donors were used in 15 cases. Actual patient survival is 91% 1-36 months after surgery. No patient deaths were due to technical graft failure. CONCLUSIONS: Major hepatic surgery can be accomplished with low mortality applying portal-based anatomy. Surgical precision is made possible by vascular isolation for hepatectomy and operative ultrasonography. These principles are essential for successful use of partial liver grafts in children.

Adolescent↗
PubMed1998

Use of proliferating cell nuclear antigen as a marker of liver regeneration after partial hepatectomy in rats.

In order to document and compare proliferating cell nuclear antigen (PCNA) mRNA and protein levels with more traditional parameters of hepatic regenerative activity in a rat model, adult male Sprague-Dawley rats (4 to 6 per group) were killed at various times up to 96 hours after 70% partial hepatectomy. At each time interval, tissue PCNA mRNA abundance and protein levels were documented (by Northern and Western blot analysis, respectively) and compared with the results of PCNA immunostaining and 3H-thymidine incorporation into hepatic DNA. Tissue PCNA protein levels were also documented in additional groups of rats 12, 24, 36, and 48 hours after sham or 30% partial hepatectomy. PCNA mRNA expression after partial hepatectomy was variable: almost undetectable at 24 hours, levels returned to baseline at 36 hours, then fell again to low levels at 96 hours. PCNA protein levels remained stable for 36 hours, increased to fourfold above baseline (p < 0.01) at 48 hours, then remained elevated for the duration of the 96-hour study. Changes in PCNA by immunostaining were similar but tended to occur somewhat earlier (significant increases being detectable at 24 hours), whereas 3H-thymidine incorporation detected the earliest increases in DNA synthesis at 12 hours and peaked at 36 hours. Peak PCNA protein levels correlated with the extent (0%, 30%, or 70%) of hepatic resection. The results indicate that PCNA protein level as determined by Western blot analysis, but not PCNA mRNA expression, correlates with PCNA immunostaining and 3H-thymidine incorporation in the regenerating liver. These findings support the use of PCNA protein determinations as an additional quantitative measure of hepatic regenerative activity after partial hepatectomy in rats.

Animals↗
PubMed2003

BCL-2 and BAX expression and cell proliferation, after partial hepatectomy with and without ischemia, on cholestatic liver in rats: an experimental study.

BACKGROUND: Liver regeneration after partial hepatectomy (PHx) is regulated by several factors that activate or inhibit hepatocyte proliferation. Apoptosis seems to play an important role in cellular proliferation and liver regeneration. This study investigates the expression apoptosis-associated genes bcl-2 and bax, and the presence of apoptosis and cell proliferation after PHx, in normal and jaundiced rats with or without superimposed ischemia. MATERIALS AND METHODS: The study included 50 male Wistar rats assigned into; five groups (10 rats each). On day 0, rats of groups II, IV, and V underwent common bile duct ligation (BDL). On day 10, total liver ischemia (TLI) (occlusion of hepatic artery and portal vein-TLI) for 30 min was performed on animals of group V. When TLI was completed, all 30 animals (of groups I, IV, and V) underwent PHx (68%). Animals of group III underwent only TLI for 30 min. Rats of groups I, IV, and V were sacrificed 24 and 48 h after PHx was completed. Rats of group II were sacrificed 10, 11, and 12 days after BDL. Rats of group III were sacrificed immediately, 24 and 48 h after TLI completion. Liver tissue was obtained and pathologic examination included: (a) H&E stain, (b) in situ hybridization (detection of bcl-2 and bax mRNA) in paraffin sections, (c) Western blot analysis for the evaluation of bcl-2 and bax protein levels, (d) in situ hybridization (TUNEL) for the detection of apoptotic bodies, and (e) immunohistochemical stains (streptavidin-biotin method) in paraffin sections to detect cells that (i) express bcl-2 and bax proteins and (ii) undergo proliferation (Ki67+ cells). Results were expressed following morphometric analysis. RESULTS: Before hepatectomy, bcl-2 (protein or mRNA) levels were higher in jaundiced rats vs controls. Furthermore, bax (protein or mRNA) levels and apoptotic body index (ABI) were higher in cholestatic livers. After hepatectomy, there was an early decrease in the protein and mRNA levels of antiapoptotic gene bcl-2 and a late increase of proapoptotic gene bax and the ABI, compared to controls. Cell proliferation of hepatocytes was lower in group V (BDL + TLI) compared to that of groups II and IV (BDL). CONCLUSIONS: This study shows that apoptosis takes place in cholestatic livers with or without superimposed ischemia and may contribute in the impaired regenerative response observed in livers of jaundiced rats after partial hepatectomy.

Animals↗
PubMed1999

Dehydroepiandrosterone (DHEA) facilitates liver regeneration after partial hepatectomy in rats.

In this study we investigated whether or not liver regeneration is facilitated by dehydroepiandrosterone (DHEA) after partial (70%) hepatectomy in rats. Treatment with DHEA (300 mg/kg body weight) did not cause any significant increase in the expression ratio of proliferating cell nuclear antigen (PCNA) in sham-operated controls; however, in partially hepatectomized rats it caused a significant increase in the ratio in hepatocytes 24 and 36 hr after hepatectomy. In partially hepatectomized rats, DHEA treatment significantly accelerated the restoration of liver 48, 60, and 72 hr after partial hepatectomy. The restoration rate in DHEA-treated hepatectomized rats at 72 hr was 1.3-fold greater than in partially hepatectomized controls. Treatment with androstenedione (300 mg/kg body weight), the first metabolite of DHEA, did not cause any significant increase in the expression of PCNA in either sham-operated controls or partially hepatectomized rats. These results indicate that DHEA itself promotes the liver regenerative process after partial hepatectomy in rats.

Androstenedione↗
PubMed1997

A new technique of one-stage total hepatectomy in the rat.

BACKGROUND: A small animal model of one-stage total hepatectomy is needed for the study of the consequences of fulminant liver failure and to investigate the extrahepatic metabolism of drugs metabolized by the liver. The models of hepatectomy described previously in the rat have the disadvantage of multiple stages, technical difficulty, or achievement of only an incomplete removal of the liver tissue. METHODS: A Y-shaped graft was prepared from the inferior vena cava and the left renal vein of a donor rat. A total hepatectomy was performed in a recipient rat. The graft was placed and the portorenal and lower cavocaval anastomoses were performed by means of the polyethylene cuff technique. The upper cavocaval anastomosis was fashioned with a continuous suture. The procedure was performed on 49 rats, and the animals were studied for survival and biochemical profiles. RESULTS: The surgical procedure took a mean of 40 +/- 5 minutes and was not associated with any operative deaths. The portal clamping time did not exceed 15 minutes. Spontaneous mean survival of the anhepatic rats was 360 +/- 30 minutes, and glucose supplemented animals had a mean survival time of 20 +/- 5 hours. The anhepatic state was associated with significant metabolic and biochemical alterations. CONCLUSIONS: This procedure is quick to perform and does not require considerable microsurgical expertise. It provides a reproducible small animal model of total hepatectomy that is particularly useful for metabolic studies.

Animals↗
PubMed2000

Activated protein C prevents multiple organ injury following extensive hepatectomy in cirrhotic rats.

BACKGROUND/AIMS: Extended hepatectomy for cirrhotic liver in patients with hepatocellular carcinoma often triggers posthepatectomy liver failure. It has been shown that the microcirculatory disturbance caused by microthrombus formation and sinusoidal endothelial cellular injury is one of the causes of post-hepatectomy liver dysfunction. We therefore investigated the effect of activated protein C (APC), a potent antithrombotic serine protease with anti-inflammatory effects, on posthepatectomy liver dysfunction and multiple organ injury in cirrhotic rats. METHODS/RESULTS: Dimethylnitrosamine-induced cirrhotic rats underwent 70% hepatectomy and received lipopolysaccharide (200 microg/kg) 48 h later to prepare a lethal posthepatectomy acute liver failure model. APC (1500 U/kg), given intravenously 15 min before and 1 h after endotoxin challenge, attenuated liver dysfunction and decreased serum tumor necrosis factor-alpha concentration. APC significantly improved the survival rate of rats at 12 h after endotoxin challenge. Histological examination revealed that APC treatment inhibited not only intrasinusoidal fibrin deposition and massive hepatocellular necrosis but also pulmonary injury and glomerular fibrin deposition. Immunohistochemically, expression of intercellular adhesion molecule-1 on sinusoidal cells and renal glomeruli was decreased in the APC-treated animals. CONCLUSIONS: APC administration prevented acute liver dysfunction and attenuated multiple organ injury following extended hepatectomy in cirrhotic rats, possibly via anticoagulant and anti-inflammatory effects.

Animals↗
PubMed2002

Inhibition of urokinase-type plasminogen activator delays expression of c-jun, activated transforming growth factor beta 1, and matrix metalloproteinase 2 during post-hepatectomy liver regeneration in mice.

BACKGROUND/AIMS: Although urokinase-type plasminogen activator (u-PA) is suggested to initiate various factors in liver regeneration after hepatectomy, no corroborative evidence has been reported. In the present study, we investigated the effect of u-PA on liver regeneration after hepatectomy. METHODS: Mice were placed into either a control group or a u-PA-inhibited group that received an in vivo u-PA inhibitor, p-aminobenzamidine. After we had removed two-thirds of the liver, we examined the expressions of c-jun mRNA and activated transforming growth factor beta 1 (TGF-beta 1), matrix metalloproteinase-2 (MMP-2) activity, and the level of hepatocyte and non-parenchymal cell proliferation in the two groups. RESULTS: In the u-PA-inhibited group, the delays in c-jun mRNA expression, hepatocyte proliferation, activated TGF-1 expression, and expression of MMP-2 activity, were 2h, 1, 2, and 1 day, respectively, and the sinusoid architecture was not restored by 10 days after hepatectomy. CONCLUSIONS: u-PA inhibition delays the expression of c-jun mRNA, hepatocyte proliferation, and restoration of the sinusoid architecture, suggesting that u-PA plays important roles in liver regeneration after hepatectomy through control of a transcription factor, c-jun expression.

Animals↗
PubMed2002

Steatosis is not sufficient to cause an impaired regenerative response after partial hepatectomy in rats.

BACKGROUND/AIMS: Fatty liver is known to be associated with increased mortality and morbidity after liver resection. The ability of fatty liver to regenerate after two-thirds partial hepatectomy was studied in three different models of steatosis in rats: obese Zucker rats, orotic acid-fed Wistar rats and Wistar rats fed a methionine-low, choline-deficient diet. METHODS: Liver regeneration was assessed 24 h after partial hepatectomy by bromodeoxyuridine incorporation (immunohistochemistry), proliferating cell nuclear antigen, cyclin E and cyclin-dependent kinase 2 protein expression (Western blot analysis) and cyclin-dependent kinase 2 activity (kinase assays using histone H1 as a substrate). RESULTS: No significant difference of proliferative response was found between orotic acid or methionine-low, choline-deficient diet-fed and control Wistar rats 24 h after partial hepatectomy. In contrast, hepatocyte proliferation in obese Zucker rats after partial hepatectomy was significantly reduced when compared with their lean controls. CONCLUSIONS: Steatosis per se does not impair liver regeneration. The reduced liver regeneration observed in obese Zucker rats may not be due to fatty infiltration itself but to other factors such as leptin receptor dysfunction.

Animal Feed↗
PubMed2003

Mitochondrial glutathione content determines the rate of liver regeneration after partial hepatectomy in eu- and hypothyroid rats.

BACKGROUND/AIMS: Mitochondrial glutathione has been postulated to affect mitochondrial function and liver regeneration. METHODS: Mitochondrial respiration, total and oxidized glutathione, and liver regeneration were assessed after partial hepatectomy in glutathione-depleted and in hypothyroid rats with/without supplementation of glutathione ester. RESULTS: Mitochondrial, cytosolic and circulating glutathione levels were lower in glutathione-depleted rats. Hepatectomy was followed by significant changes of intra- and extracellular glutathione and of mitochondrial respiration. In glutathione-deficient rats, the recovery of mitochondrial function and the liver regeneration were delayed. Administration of glutathione ester partially corrected the fall of cytosolic and mitochondrial glutathione following hepatectomy, reduced mitochondrial oxidative damage, and accelerated the restoration of mitochondrial respiration and the rate of liver regeneration. In hypothyroid rats, intracellular glutathione homeostasis and mitochondrial respiration were impaired already at baseline; slower regeneration and mitochondrial oxidative alterations were observed after hepatectomy. Glutathione ester ameliorated the regenerative response in hypothyroid rats by providing higher concentrations of cytosolic and mitochondrial glutathione. CONCLUSIONS: Glutathione depletion and hypothyroidism affect the mitochondrial function during liver regeneration. Liver regenerates more slowly in glutathione-depleted and in hypothyroid rats. The earlier restoration of mitochondrial function and the higher rate of proliferation in glutathione ester treated rats suggest that the maintenance of intracellular glutathione facilitates liver regeneration.

Animals↗
PubMed1993

Distribution and activity of glutamine synthase and carbamoylphosphate synthase upon enlargement of the liver lobule by repeated partial hepatectomies.

Glutamine synthase and carbamoylphosphate synthase show a strikingly heterogeneous and fully complementary distribution in the rat liver. In the human liver, however, there is a midlobular zone where both enzymes are absent. The diameter of the human liver lobule is approximately twice the size of the rat lobule. To investigate whether lobule size is a major determinant for the expression patterns of glutamine synthase and carbamoylphosphate synthase, Wistar strain rats were partially hepatectomized 3 times, at weekly or monthly intervals. Due to hepatic regeneration the cross-sectional area of the liver lobules increased twofold. However, a midlobular zone which lacked expression of both glutamine synthase and carbamoylphosphate synthase did not develop in these livers, thus showing that lobular size is not a major determinant for the distribution patterns of glutamine and carbamoylphosphate synthase. The twofold increase in the cross-sectional area of the liver lobule was associated with a similar reduction in the relative number of glutamine synthase-positive cells and in the enzyme content of the liver, indicating that the regeneration process does not affect the pericentral pattern of glutamine synthase expression. After regeneration was complete, the glutamine synthase content in the liver was restored to its original value, demonstrating a twofold increase in the cellular concentration of glutamine synthase-positive hepatocytes. An increase in the diameter of the liver lobule was only seen after the first partial hepatectomy. Liver growth following subsequent partial hepatectomies can be explained by an increase in the length of the liver lobule and/or by splitting of liver lobules. The zonal distribution of DNA replication, which is characteristic of the first partial hepatectomy, is lost after repeated partial hepatectomies. Furthermore, evidence was obtained that the signal for inducing DNA synthesis may originate at the level of single liver units.

Animals↗
PubMed1986

Hepatic regenerative stimulator substance in the rabbit. Relation to liver regeneration after partial hepatectomy.

The occurrence and activity of hepatic regenerative stimulator substance was investigated in the partially hepatectomized rabbit and related to biochemical and morphological parameters of liver regeneration. Male rabbits were 60% hepatectomized by excising the Spigelian, left lateral and left central lobes of the liver leaving the gallbladder in situ. [3H]Thymidine incorporation into DNA, the fraction of labelled hepatocyte nuclei, the fraction of mitoses and thymidine kinase activity rose from basal levels at 30-40 h after hepatectomy and increased up to 12-fold at 40-60 h. After 7 days, proliferation parameters returned to near prae-hepatectomy values and 82% of the initial liver mass was restored. Hepatic regenerative stimulator substance was biologically active when prepared from rabbit livers between 18-30 h after partial hepatectomy. At 12 and 30 h after intraperitoneal injection of the extract into normal rats, hepatic DNA synthesis was stimulated up to 2-fold in a dose-dependent fashion. The biological activity was protease-sensitive and thus depended on a protein component of the extract. The data demonstrate the existence of hepatic regenerative stimulator substance in regenerating rabbit liver and suggest that it is implicated in the regulation of liver growth after partial hepatectomy.

Animals↗
PubMed1997

Stimulation of liver regeneration and function after partial hepatectomy in cirrhotic rats by continuous infusion of recombinant human hepatocyte growth factor.

BACKGROUND/AIMS: Radical resection is accepted as one of the most curative treatments for hepatocellular carcinoma. However, most patients have coexisting cirrhosis and their liver function is usually impaired. It is therefore important to stimulate the regeneration and function of the remnant cirrhotic liver after hepatectomy. Hepatocyte growth factor is a potent mitogen that has been suggested to play a crucial role in liver regeneration. METHODS: In this study, we performed 45% hepatectomy in rats with cirrhosis induced by thioacetamide, and administered recombinant human hepatocyte growth factor (rhHGF) with dextran sulfate by continuous infusion into the jugular vein with an infusion pump. RESULTS: rhHGF stimulated an increase in the wet weight of the remnant liver compared with untreated control rats. The proliferating cell nuclear antigen labeling index showed that this increase resulted from the stimulation of DNA synthesis. Serum levels of liver enzymes increased after hepatectomy, but returned to the prehepatectomy level more rapidly in rhHGF-treated rats than in controls. rhHGF increased hepatic protein synthesis above prehepatectomy levels and also markedly increased the serum levels of hepatic lipid metabolites. CONCLUSIONS: These results demonstrate that continuous intravenous infusion of rhHGF enhances the growth and function of the remnant liver in rats with cirrhosis after partial hepatectomy. Therefore, rhHGF may be useful after hepatic resection in patients with cirrhosis.

Animals↗
PubMed1997

Changes in expression of CCAAT/enhancer binding protein alpha (C/EBP alpha) and C/EBP beta in rat liver after partial hepatectomy but not after treatment with cyproterone acetate.

BACKGROUND/AIMS: The proliferation rate of adult rat liver is normally very low. It is markedly enhanced during compensatory regeneration, e.g. after partial hepatectomy, or after administration of certain growth promoters, e.g. cyproterone acetate. These two types of liver cell proliferation appear to differ, since the expression of immediate early genes is induced during compensatory regeneration but not after cyproterone acetate treatment. The transcription factor C/EBP alpha, which has been associated with hepatocyte differentiation and growth arrest, is suppressed during compensatory regeneration. In contrast, C/EBP beta, associated with acute phase reaction, is increased during regeneration. We have investigated the effects of the liver growth promoter cyproterone acetate on the hepatic expression of C/EBP alpha and C/EBP beta. METHODS: Adult male rats received either cyproterone acetate treatment or were subjected to partial hepatectomy. Livers were obtained at different time intervals for measurement of C/EBP alpha and C/EBP beta mRNA with solution hybridization/RNAse protection assay, and C/EBP alpha and C/EBP beta content with immunoblotting. RESULTS: The levels of both C/EBP alpha and C/EBP beta mRNA and the corresponding immunoreactivities were unchanged 2-48 h after injection of cyproterone acetate. The levels of C/EBP alpha mRNA and immunoreactivity were significantly suppressed 10-18 h and 18-26 h after partial hepatectomy, respectively. The levels of C/EBP beta mRNA and immunoreactivity were enhanced during compensatory regeneration 2 h after partial hepatectomy. CONCLUSIONS: Liver cell proliferation during regeneration, but not in response to cyproterone acetate treatment, is associated with changes in C/EBP alpha and C/EBP beta expression. This further supports the notion that changes in expression of transcription factors during liver growth in vivo are dependent on the growth inducer.

Animals↗
PubMed1998

Augmentation of the early phase of liver regeneration after 70% partial hepatectomy in rats following selective Kupffer cell depletion.

BACKGROUND/AIMS: Kupffer cells are located in the liver sinusoids adjacent to hepatocytes and elaborate a range of growth regulatory molecules involved in regulating hepatocyte proliferation. In vitro observations imply the potential for Kupffer cells to exert both stimulatory and inhibitory influences on hepatocyte DNA synthesis. We aimed to determine the overall effect of Kupffer cell activity during the early regenerative processes after partial hepatectomy. METHODS: We investigated hepatocyte DNA synthesis, induced by partial hepatectomy in rats, following selective elimination of Kupffer cells by liposome encapsulated dichlormethylene bisphosphonate (Cl2MBP). RESULTS: We demonstrate that the early phase of liver regeneration was enhanced following Kupffer depletion, as indicated by a greater proportion of hepatocytes undergoing DNA synthesis, and a higher mitotic index. This was associated with an alteration in the balance of growth factors in the liver; HGF and TGFbeta mRNA were reduced in Kupffer cell-depleted animals, and IL-1beta mRNA was absent. In addition, in the absence of partial hepatectomy, the selective depletion of Kupffer cells leads to an increase in the proliferation of hepatocytes in resting liver undergoing DNA synthesis. CONCLUSION: The overall effect of depleting the liver of Kupffer cells is to enhance the proliferation rate of hepatocytes, both after partial hepatectomy and in the resting state.

Animals↗
PubMed1999

Effects of glutamine administration on liver regeneration following hepatectomy.

The intestine is now known to be an important site of protein production in the body, and glutamine (GLN) stimulates both secreted and non-secreted protein synthesis in the small bowel. The purpose of the present study was to evaluate the effect of GLN-supplemented parenteral nutrition on liver regeneration after hepatectomy. Animals were divided into two groups: a sham-operated control group (Group A) and a 70%-hepatectomy group (Group B). Postoperatively, one-third of the animals in each group were maintained on intravenous 10% glucose solution, on 10% glucose with 2% standard amino acid solution, or 10% glucose supplemented with 2% glutamine for 24 h. GLN administration after hepatectomy significantly promoted liver regeneration. In addition, assessment of amino acid metabolism showed that GLN administration activated GLN metabolism in the intestine and promoted alanine uptake by the remnant liver. This metabolic response also enhanced both secreted and non-secreted protein synthesis in intestinal epithelial cells, especially in cells isolated from the crypts. The proteins produced are important as a portal production factor for liver regeneration and intestinal cell proliferation. Bacterial and endotoxin translocation, on the other hand, was significantly reduced. Thus, the results of this study suggest that intravenous administration of GLN after hepatectomy significantly promoted liver regeneration.

Amino Acids↗
PubMed1998

Safety of selective vascular clamping for major hepatectomies.

BACKGROUND: Although hepatic vascular clampings are widely used during major hepatic resections, they may not always be necessary. Selective vascular clamping, which only controls the afferent blood flow of the resected liver, could be a valuable alternative, provided that blood loss is not increased because the opposite liver remains perfused. STUDY DESIGN: The aim of the study was to assess the safety of selective vascular clamping in 43 patients who underwent 36 right hepatectomies and 7 left hepatectomies for lesions located peripherally within the liver. Blood transfusions, hepatic tests, morbidity, mortality, and hospital stay were evaluated. RESULTS: Selective vascular clamping was efficient in 34 of the 43 attempts (79%), but bleeding from the contralateral liver required conversion to portal triad damping in 9 patients (21%). Median blood transfusions were 0 units (range 0 to 4 U), and 28 patients (65%) did not require transfusions. Postoperative laboratory tests showed that larger changes occurred at day 1 and tended to return to preoperative values at the end of the first postoperative week. Median time of hospitalization was 10 days (range 7 to 28 days). Postoperative course was uneventful in 35 patients (81%). Nonlethal complications occurred in 7 patients (16.3%). One patient (2%) with massive hepatic steatosis died of liver failure after right hepatectomy. CONCLUSIONS: Selective vascular clamping is a safe alternative to total inflow occlusion for major hepatectomies applicable in 80% of selected patients with peripheral liver tumors.

Adult↗
PubMedDate not supplied

Kupffer cell-mediated inhibition of liver regeneration after combined hepatectomy and pancreatectomy.

Recently, simultaneous hepatectomy and pancreatoduodenectomy has been performed for the treatment of some biliary tract cancers in Japan. Postoperative hepatic failure is a common and potentially fatal complication. The aim of this study was to examine the reduction in the rate of liver regeneration after 70% hepatectomy (Hx) alone or in combination with 70% pancreatectomy (HPx). Male Sprague-Dawley rats underwent hepatectomy or simultaneous hepatectomy and pancreatectomy. The ratio of liver weight to body weight, the labeling index of hepatocytes in vivo, and DNA synthesis of the hepatocytes and/or Kupffer cells in primary culture were analyzed. The ratio of liver weight to body weight and the labeling index in HPx rat were found to be significantly lower than those values in Hx rats. There were no significant differences in plasma alanine aminotransferase levels between the two groups. The inhibitory effect on DNA synthesis was observed with coculture of hepatocytes and Kupffer cells when the portal plasma obtained 1 hour after operation was added. We further observed that the conditioned medium of Kupffer cells stimulated by the addition of the portal plasma that was obtained 1 hour after HPx inhibited DNA synthesis of hepatocytes. This effect was abolished after incubation at 56 degrees C for 30 minutes. These results strongly suggest the existence of a growth inhibitory factor in portal plasma after HPx. This heat-labile growth inhibitory factor was released from Kupffer cells and would appear to act on hepatocytes in a paracrine manner.

Animals↗
PubMed2000

Correlation between decreased expression of mitochondrial F0F1-ATP synthase and low regenerating capability of the liver after partial hepatectomy in hypothyroid rats.

In hypothyroid rats, partial hepatectomy does not induce liver regeneration until 120 h after surgical operation. when, instead, in normal rats a complete recovery of the liver mass, in this interval, is observed. In normal rats, a good efficiency of mitochondrial oxidative phosphorylation is needed as an energy source for liver regeneration (Guerrieri, F. et al., 1995); in hypothyroid rats the efficiency of mitochondrial oxidative phosphorylation is low in the 0-120 h interval after partial hepatectomy. This low efficiency of oxidative phosphorylation appears to be related to a low mitochondrial content of F0F1-ATP synthase, in liver of hypothyroid rats, which does not recover after partial hepatectomy. In the liver of hypothyroid rats, low levels of the nuclear-encoded mitochondrial catalytic betaF1 subunit and of its transcript are observed and they do not increase, as occurs in normal rats, after partial hepatectomy.

Adenosine Triphosphate↗