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PubMed1990

Lysosomal redistribution and increased fragility of pancreatic acinar cells in early stage after hepatectomy in rats.

To explore the cellular fragility of pancreatic acinar cells in the early stage after partial hepatectomy, we evaluated the subcellular redistribution of lysosomal enzyme, lysosomal fragility in acinar cells, lactate dehydrogenase (LDH) discharge from acinar cells and the pancreatic water content in rats 4 days after about 70% hepatectomy. Following hepatectomy, there was redistribution of lysosomal enzymes, and more cathepsin B in zymogen pellets (1.3 KP) and less cathepsin B in lysosomal pellets (12 KP) than in sham-operated or normal rats. Soluble cathepsin B activity and LDH discharge also increased significantly after hepatectomy. The pancreatic water content was significantly increased after hepatectomy. These results indicate that the fragility of acinar cells increased in the early stage after hepatectomy.

Animals↗
PubMed1989

[The significance of lipid peroxidation (free radical) on hepatocellular dysfunction following hepatectomy].

The possibility of extended hepatectomy was examined clinically and experimentally, with special reference to relation between remnant liver dysfunction and lipid peroxidation. Clinical study: When the functional reserve of the remnant liver prior to hepatectomy was below the critical level, both serum phospholipase A2 and plasma lipid peroxide increased and severe hepatic insufficiency occurred. Experimental study in dogs: The amount of lipid peroxide in the plasma and remnant liver increased more after 84% hepatectomy than after 70% hepatectomy, causing significant impairment of the remnant liver function. To prevent hepatic dysfunction after hepatectomy, Coenzyme Q10, an antioxidant and a membrane stabilizer, were administered. These substances reduced the increase of lipid in the plasma and remnant liver, and restored the liver function with subsequent good regeneration. The results suggest that the administration of Coenzyme Q10 may be useful for recovery of liver function and a more favorable prognosis following the extended hepatectomy.

Animals↗
PubMed1989

Regenerative enzyme activity of the liver after partial hepatectomy or toxic injury depressed by continuous NH4+ infusion.

Persistent slight or modest increments in blood ammonia level resulting from continuous intravenous infusion of NH4+ depressed hepatic thymidine kinase (TK) activity (DNA synthesis) by 30% after two-lobe (70%) hepatectomy, by 32% after subtotal (90%) hepatectomy, by 80% after massive injury with 1400 mg/kg acetaminophen, and by 92% after massive injury with 1000 mg/kg galactosamine. Ornithine decarboxylase activity (reflecting initiation of regeneration) was similarly depressed by 65% after 70% hepatectomy, by 58% after acetaminophen, and by 87% after galactosamine. It was not depressed after 90% hepatectomy. Intermittent marked but transient increments in blood ammonia level resulted in similar but slightly smaller enzyme reductions after the injuries with the toxins, and a reduction of 92% in TK activity after 70% hepatectomy. Thus, after toxic injury, both regenerative enzymes were substantially depressed by excess ammonia, whether present transiently in large amounts or persistently in small amounts. After partial hepatectomy, TK activity was similarly depressed by the large transient amounts of ammonia but was less affected by the persistent smaller amounts.

Acetaminophen↗
PubMed1985

[Cyclic AMP response to glucagon after partial hepatectomy].

To clarify the functional recovery of the liver after partial hepatectomy, serum c-AMP responses to glucagon were investigated after hepatectomy in rats. Serum glucagon, insulin and weight of the regenerating liver were simultaneously measured. Wistar strain male rats, weighing 120-130 g, were divided into three groups; I 30% hepatectomy, II 70% hepatectomy and III sham operation. On the first postoperative day, cyclic AMP response to glucagon was remarkably decreased in I and II groups. In group I, c-AMP response returned to the normal level 2 weeks after operation. In group II the response returned to normal at the sixth postoperative week. The liver weights were almost normal after two weeks in the both groups. Levels of serum glucagon sharply increased 24 hours after operation and returned to the normal level after 7 days. However the levels of serum insulin showed no remarkable changes. In conclusion, the complete functional recovery of the liver after hepatectomy needed 6 weeks in cyclic AMP response to glucagon and was delayed 4 weeks to that of the liver weight after 70% hepatectomy. Insulin seems to have no direct effect of the liver regeneration.

Animals↗
PubMed1988

[Experimental study on lipid metabolism after partial hepatectomy--with reference to mitochondrial function of the regenerating liver].

Lipid metabolism after hepatectomy was studied in normal rats and cirrhotic rats induced with injections of thioacetamide. In normal rats, the fat accumulation in regenerating livers was observed, which had a maximal peak at 24 hours after hepatectomy. It could be a result of mobilization of fatty acids from fat tissue accompanied with hyperglucagonemia after hepatectomy. Mitochondrial respiration in regenerating liver increased remarkably. Especially when palmitoylcarnitine was used as a substrate, both the respiratory index and ATP synthesis were high until 72 hours after hepatectomy. Mitochondrial carnitine palmitoyltransferase activity was also high. The increase of mitochondrial respiration with palmitoylcarnitine as a substrate was also observed in cirrhotic liver until 72 hours after hepatectomy. These results suggest that mobilization of fatty acids increases after hepatectomy and regenerating liver utilizes fatty acids as a main substrate for hepatic regeneration.

Animals↗
PubMed1987

[Experimental study on the development of acute gastric ulcer after hepatectomy in liver cirrhosis--mainly changes in the gastric wall protection mechanism].

Gastric wall blood flow, gastric mucosal noradrenalin (NA), gastric mucosal prostaglandin E2 (PGE2) and gastric mucosal energy metabolism were studied after partial hepatectomy in thioacetamide (TAA) --induced cirrhotic rats and these were also tested by loading water immersion restraint on the 3rd day after partial hepatectomy. Furthermore, the preventive effects of PGE2 on ulcers were also examined. Liver cirrhosis rats were prepared with an abdominal administration of TAA three times a week for 10 weeks, after which 70% partial hepatectomies were performed. The results of these tests showed that the gastric mucosa after partial hepatectomy in liver cirrhosis rats had significantly lower gastric wall blood flow, gastric mucosal NA and gastric mucosal energy and reduced gastric mucosal PGE2. The water immersion restraint stress loaded on the 3rd day to these rats after partial hepatectomy caused a noticeable and an earlier reduction in gastric wall blood flow and gastric mucosal PGE2 than to the normal group, and the ulcer index was high. PGE2 administration also appeared to be effective for the prevention of development of acute ulcers after partial hepatectomy in liver cirrhosis rats.

Acute Disease↗
PubMed1987

[Ultrastructural changes in the hepatocytes following massive hepatectomy in rats].

This study was carried out to investigate the ultrastructural changes of the hepatocytes of the remnant liver after 70% hepatectomy in rats. The remnant liver regained the preoperative weight one week after hepatectomy. During this early posthepatectomy period, the volume of the each hepatocytes increased to a peak 48 hours after hepatectomy, then returned to normal within one week. Electronmicroscopically mitochondria of the hepatocytes became swollen and the cristae were shortened until 3 hours after hepatectomy. Dividing mitochondria were also observed in the initial 2 hours. The volume density of the mitochondria measured as a percentage of the mitochondrial volume per the cytoplasmic volume of hepatocytes. It increased and reached a peak 3 hours after hepatectomy (p less than 0.05) and thereafter returned to the same value as the control within 6 hours. Then it gradually decreased until 7th day (p less than 0.001). The volume density of lipid droplets increased to a peak 48 hours after hepatectomy (p less than 0.01). These significant ultrastructural changes of the hepatocytes indicate an important roles of mitochondria especially in the energy metabolism in the early posthepatectomy period.

Animals↗
PubMed1987

[Effects of preoperative transcatheter arterial embolization (TAE) on the liver following partial hepatectomy in rats].

The safety of pre-operative transcatheter arterial embolization (TAE), especially on the relation to hepatic regeneration following partial hepatectomy, was evaluated in rats. TAE was done through a catheter cannulated into hepatic artery under laparotomy. The remarkable elevation of S-GOT and S-GPT levels were demonstrated a day after TAE, which returned to normal on third post operative day. No influence of the difference of embolized materials was seen on the changes of transaminase levels. TAE severely decreased hepatic microsomal functional mass measured by [14C]-aminopyrine breath test (ABT) and the recovery of microsomal functional mass was shown on the 14th day after TAE. Histologically, recanalization could not be revealed in embolized arterioles even on the 21st day after TAE. But trabecular pattern of hepatic lobules was preserved after TAE. The serious inhibition of DNA synthesis of regenerating liver was demonstrated when TAE was performed within 14 days prior to partial hepatectomy (p less than 0.001-0.05). The period from TAE to partial hepatectomy had a influence on the survival rate after partial hepatectomy, and when appropriate interval was taken after TAE, the survival rate increased significantly (33%-50% in 24 hours interval and 88% in 14 days interval). In conclusion, preoperative TAE remarkably suppressed hepatic regeneration after partial hepatectomy, and appropriate time when suppressed hepatic functional mass, such as microsomal functional mass measured by ABT, returned to pre TAE value was required to perform hepatectomy in safety.

Animals↗
PubMed1971

Effects of partial hepatectomy in rats on two transplantable hepatomas. Changes in weight and in synthesis of DNA and ferritin.

Partial hepatectomy in rats carrying Reuber H-139 and H-35 hepatomas is followed by rapid growth of these tumors. At comparable times after implantation, average wet weights of H-139 or H-35 hepatomas in partially hepatectomized rats were significantly higher than average wet weights of these tumors in control rats. In H-35 hepatomas growing subcutaneously, synthesis of DNA, as shown by incorporation of tritiated thymidine, was depressed 18 hours after a two-thirds hepatectomy in the host. Between 18 and 36 hours after partial hepatectomy, DNA synthesis rose steadily, with a maximum at about 36 hours. Incorporation of (14)C-leucine into ferritin (apoferritin) reached a maximum in liver and, to less extent, also in subcutaneous H-35 hepatomas, 48 hours after partial hepatectomy and returned to normal levels at 72 hours. The increase in wet weight of the tumors is most likely the result of an increase in rate of growth concomitant with the restoration of liver mass. The rise in synthesis of DNA and of ferritin in hepatoma cells after partial hepatectomy suggests that these hepatomas were affected by the same humoral factor or mechanism that stimulates cell division and protein synthesis in the liver immediately after partial hepatectomy.

Animals↗
PubMed1984

Time-courses of hepatocellular hyperpolarization and cyclic adenosine 3',5'-monophosphate accumulation after partial hepatectomy in the rat. Effects of fasting for 48 hours and intravenous injection of glucose.

Hepatic cell membrane potentials, hepatic cyclic adenosine 3',5'-monophosphate concentrations, and blood glucose levels were measured in anesthetized rats before, and at various times after, partial hepatectomy. In fed rats, hyperpolarization became evident 1-3 h postoperatively, reached its first peak at 4 h, and was maintained for approximately 36 h. The early phase of hyperpolarization was preceded by depletion of glycogen from the liver remnant and occurred during a decline of blood glucose concentrations below the level in sham-operated rats. Preoperative exhaustion of glycogen stores by fasting for 48 h resulted in marked hyperpolarization within 15 min after partial hepatectomy. In fasted rats, an intravenous injection of glucose (10 mmol X kg-1) caused a delay in hyperpolarization when given 30 min before partial hepatectomy, or a transient normalization of the membrane potentials when given 30 min after partial hepatectomy. Liver tissue cyclic adenosine 3',5'-monophosphate concentrations in fed rats remained largely unchanged 2 h after partial hepatectomy but increased greatly at 4 h. On the other hand, in fasted rats a significant increase was seen within 30 min. Glucose administration to fasted rats depressed cyclic adenosine 3',5'-monophosphate concentrations in the liver remnant. The results suggest that intensified gluconeogenesis, partly mediated by cyclic adenosine 3',5'-monophosphate, could be the event underlying early hepatocellular hyperpolarization induced by partial hepatectomy.

Animals↗
PubMedDate not supplied

[Coagulation disturbances after subtotal or total hepatectomy in the dog (author's transl)].

The authors relate 15 cases of blood coagulation disturbances among three groups of animals after 80%, 90% or total hepatectomy. Animals in group I, after 80% hepatectomy, were sacrified between the 10th and 30th postoperative days. Group II animals, with 90% hepatectomy, survived for periods ranging from 18 to 24 hours. In group III, after total hepatectomy, survival varied between 30 and 40 hours. The coagulation disturbances which were observed following 80% hepatectomy were spontaneously compatible with the survival of the animals. Following 90% and total hepatectomy the resulting disturbances were constantly severe enough to limit survival time. Supportive procoagulant therapy associated with sequential heparin administration seems justified by the insufficient biosynthesis of clotting factors and their unavoidable consumption as a result of localized then disseminated intravascular coagulation and secondary fibrinolysis.

Animals↗
PubMed1981

Differences in predominant energy substrate in relation to the resected hepatic mass in the phase immediately after hepatectomy.

Changes in the energy substrate utilized by the remnant liver after hepatectomy were studied in relation to the hepatic energy status in 25%, 70%, and 93% hepatectomized rabbits. In 25% hepatectomized rabbits, the energy charge ((ATP + 1/2ADP)/(ATP + ADP + AMP)) level of the remnant liver remained unchanged after hepatectomy and was not affected by portal infusion of (+)-octanoylcarnitine, an inhibitor of fatty acid oxidation. In contrast, the energy charge level of the remnant liver decreased rapidly after 70% hepatectomy and reached the lowest level of 0.77 at 12 to 24 hr after hepatectomy (p less than 0.01). At this time, the energy charge level was further decreased to 0.45 by (+)-octanoylcarnitine (p less than 0.001). It returned to near normal 4 days later. At this time, the effect of (+)-octanoylcarnitine was less evident, with the restoration of the energy change. In 93% hepatectomized rabbits, the energy charge level of the remnant liver decreased rapidly and steeply in the phase immediately after hepatectomy. It is suggested that the remnant liver metabolism switches to predominant utilization of fatty acid as an energy source when the energy charge decreases; it then becomes able to utilize glucose with the restoration of energy charge level. In addition, it is emphasized that hyperosmolar glucose solution or insulin administration during the early period after major hepatectomy should be reconsidered because of their inhibition of the mobilization of free fatty acid from adipose tissue.

Animals↗
PubMed1981

Long-term ethanol administration and short- and long-term liver regeneration after partial hepatectomy.

The purpose of this study was to determine whether long-term ethanol consumption affects the long-term regeneration of the liver after partial hepatectomy and to study whether the metabolic demands imposed on the liver by the regenerative process accentuate liver damage produced in the liver by ethanol. Animals fed alcohol (35% of total calories) in liquid diets over time were partially hepatectomized (68% removal) and then were given ethanol-containing diets until complete liver restitution. They were studied at 24 hr and at 7 and 14 days. At these times, prior and continued ethanol administration did not result in changes in total DNA restituted, percent of cells undergoing mitosis, or incorporation of 3H-thymidine into DNA as determined chemically and by autoradiography. After partial hepatectomy, ethanol-fed animals showed a reduction in both DNA and proteins per gram of liver. However, these effects were the result of the hepatomegaly induced by ethanol and were also observed in sham-operated animals fed the diets containing ethanol. An apparent decrease in percent restitution of live weight was observed at 24 hr after hepatectomy in the ethanol-fed animals. However, this was caused by a marked increase in hepatocyte size in the controls, which matched the already enlarged hepatocytes in the ethanol-fed animals. Partial hepatectomy was found to transiently increase the lipid content of the livers in control animals. In ethanol-fed animals partial hepatectomy resulted in markedly fatty livers, as observed both histologically and chemically, which exceeded these abnormalities in alcohol-fed sham-operated rats. In conclusion, long-term ethanol consumption prior to partial hepatectomy and continuous ethanol consumption after the operation did not affect negatively the complete restitution of the liver when compared with controls.

Animals↗
PubMed1995

Role of heparin-binding epidermal growth factor-like growth factor as a hepatotrophic factor in rat liver regeneration after partial hepatectomy.

Several growth factors including hepatocyte growth factor (HGF) have been implicated in the regulation of liver regeneration. Recently, we reported that heparin-binding epidermal growth factor (EGF)-like growth factor (HB-EGF) has hepatotrophic effects in vitro. We investigated the role of HB-EGF as a hepatotrophic factor in regenerating rat liver after 70% partial hepatectomy. The level of HB-EGF messenger RNA (mRNA) in regenerating rat liver increased 1.5 hours after partial hepatectomy and reached a maximum (about sevenfold over normal) at 6 hours. In contrast, hepatic HGF mRNA levels increased at 12 hours and achieved maximal expression at 24 hours. HB-EGF protein expression increased about 2.8-fold over normal at 10 hours after partial hepatectomy. The number of EGF receptors, to which HB-EGF binds, decreased 6 hours after partial hepatectomy. HB-EGF mRNA levels increased in nonparenchymal cells (NPCs) at 6 hours after partial hepatectomy but not in hepatocytes. Using the reverse transcription-polymerase chain reaction (RT-PCR), HB-EGF gene expression was increased predominantly in Kupffer cells and sinusoidal endothelial cells but not in lipocytes and hepatocytes. These results indicated that HB-EGF may be an important growth factor, produced in an earlier phase rather than HGF, in the regenerating liver after partial hepatectomy by a paracrine mechanism.

Animals↗
PubMed1993

[Changes of serum interleukin 6 (IL6) and acute phase protein after hepatectomy in patients with chronic liver disease].

We examined the changes in serum levels of interleukin 6 (s-IL6) and acute phase protein (APP) during perioperative periods in patients with or without chronic liver disease (CLD) who underwent hepatectomy or other surgeries. The elevation of s-IL6 on the first postoperative day was only correlated with preoperative values of indocyanine green retention test (ICG-R15) (r = 0.56, p < 0.01), and not concerned with any operative factors. We divided the patients into the following three groups; the patients with CLD undergoing hepatectomy (n = 21, group A), the patients without CLD undergoing hepatectomy (n = 7, group B), and the patients without CLD undergoing surgeries other than hepatectomy (n = 7, group C). The values of s-IL6 on preoperative day, 1st, 4th, and 7th days after surgery in group A were significantly higher than the corresponding values in group C (p < 0.05). Among the hepatectomy groups, the serum levels of APP on the 4th day after surgery were significantly higher than those on preoperative day. We concluded that the changes in s-IL6 after hepatectomy were strongly concerned with preoperative liver function, especially with values of ICG-R15. However, it seemed that the induction of APP was negatively correlated with the preoperative liver function.

Acute-Phase Proteins↗
PubMed1993

[Ultrastructure changes of the remnant regenerating hepatocytes after partial hepatectomy in rats].

In spite of its highly functionally differentiated characteristics, the remnant liver has the capability of regeneration after massive hepatectomy either in human beings or in experimental animals. This experiment was performed to study the ultrastructural changes of the regenerated hepatocytes after massive hepatectomy. Male Wistar rats weighing around 200g were used in this study. Partial hepatectomy with resection of the median and left lateral lobes (67.31%) was performed. The rats were sacrificed at 6, 24, 48 and 72 hours after the operation. The remnant liver was inspected under a light and electron microscope. We found that: (1) the glycogen in the cytoplasm of hepatocyte nearly disappeared 6 hours after hepatectomy, with a decrease of rough endoplasmic reticulum (RER) and an increase of smooth endoplasmic reticulum (SER) and lysosomes were noted; (2) 24 hours after hepatectomy, (the nuclear membrane became zigzag shaped and the reappearance of glycogen and an increase of RER, autophagosome and lipid droplets were noted. (3) the number of mitosis increased markedly at 48 hours postoperatively; and (4) 72 hours after hepatectomy, the lysosome and RER returned to preoperative condition with some RER became dilated; SER was hardly found and lipid droplets became bigger and increased; and the nuclear membrane shape was still a zigzag at this time.

Animals↗
PubMed1994

Proliferating cell nuclear antigen, plasma fibronectin, and liver regeneration rate after seventy percent hepatectomy in normal and cirrhotic rats.

BACKGROUND: The difference in liver regeneration rate in relation to proliferating cell nuclear antigen (PCNA) and plasma fibronectin level in the cirrhotic and control liver after 70% hepatectomy were examined in the rat. METHODS: Liver cirrhosis was induced by intraperitoneal injection of thioacetamide for 12 weeks; rats without thioacetamide administration served as controls. On the day before and days 1, 2, 3, and 7 after 70% hepatectomy, PCNA labeling index of hepatocyte, plasma fibronectin level, and percentage of the initial liver weight were determined. RESULTS: Liver regeneration rate as expressed by percent of initial liver weight was impaired in the cirrhotic liver, and significantly lower regeneration rate was observed on days 3 and 7 after hepatectomy in the cirrhotic rats as compared with controls. PCNA labeling index was higher in the cirrhotic liver before hepatectomy. Little change of PNA labeling index was observed in the cirrhotic liver, although the index increased significantly in the control liver; significantly higher values were observed on days 1, 2, and 3, with the maximal value on day 2 after hepatectomy. The plasma fibronectin level was significantly lower in the cirrhotic rat before and after hepatectomy. CONCLUSIONS: The results show that liver regeneration is impaired in the cirrhotic liver associated with little activation of PCNA and with lower plasma fibronectin level.

Animals↗
PubMed1993

[Experimental study of the time course of DNA strand breaks and DNA synthesis during liver regeneration after partial hepatectomy in rats].

The time course of DNA strand breaks (nicks) and DNA synthesis during liver regeneration were studied in rats with 70% partial hepatectomy. Cellular nicks were detected by in situ nick translation (ISNT) using biotin-labelled mixture and DNA synthesis was assessed by immunohistochemical staining using BrdU and/or PCNA monoclonal antibodies. Nicks appeared on periportal and subcapsular hepatocytes in normal liver tissue, and increased from 24 hours to 48 hours (peak time) after hepatectomy in mainly periportal area. Hepatocytes with BrdU intake increased from 24 hours after hepatectomy with peak value in mainly periportal area. Hepatocytes stained with PCNA antibody increased from 24 hours after hepatectomy in mainly periportal area and there were most positive staining cells at 48 hours after hepatectomy. In liver regeneration after hepatectomy, it apparently suggested that nicks in hepatocytes appeared in G0-G1 phase that was slightly before S phase and after M phase, but almost cells at G0-G1 were not stained, and hepatocytes with PCNA protein appeared following the BrdU intake in the same cells.

Animals↗