PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “LIVER CIRRHOSIS, EXPERIMENTAL”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1994

Decreased hepatocarcinogenic effect of diethylnitrosamine in experimentally induced liver cirrhosis in rat: delay or inhibition?

The relationship between CCl4 or (CCl4 + phenobarbital)-induced liver cirrhosis and diethylnitrosamine (DEN) hepatocarcinogenesis in male F-344 rats was investigated. DEN given alone produced no liver lesions after 16 weeks, but 4/12 (33%) neoplastic nodules developed when nitrosamine was administered to rats with previously established cirrhosis. On the other hand, (CCl4 + phenobarbital) post-treatment had an even stronger effect, increasing the yield of neoplastic nodules to 100% (28/28). Since the exposure time of DEN was the same in all treated groups (4 months), the results indicate the decreased effectiveness of (CCl4 + phenobarbital) pretreatment on DEN hepatocarcinogenesis.

Animals↗
PubMed1995

Renal endothelin system in rats with liver cirrhosis.

Rats with experimental liver cirrhosis have increased endothelin-1 (ET-1) plasma concentrations and show a tendency toward sodium and water retention. We therefore analyzed the renal ET system in cirrhotic rats and control rats, as the renal ET system is involved in the regulation of water and sodium excretion. Cirrhosis was induced by carbon tetrachloride (CCl4) administration. We analyzed the expression of ET receptor subtypes in the renal cortex and medulla using Scatchard analysis and receptor autoradiography, and measured plasma and renal tissue ET-1 concentrations using a specific radioimmunoassay. Furthermore, we analyzed the effects of the nonselective (A/B) ET receptor antagonist bosentan on water and sodium excretion and glomerular filtration rate. Our study revealed an overexpression of the ETB receptor in the renal medulla of rats with liver cirrhosis, whereas the density of ETB receptor in the cortex and the ETA receptor in the cortex and medulla were similar in both cirrhotic and control rats. Receptor autoradiography showed that the upregulation of medullary ETB in cirrhotic rats was due to an upregulation of ETB in the inner medullary collecting duct cells. The highest ET-1 concentrations were observed in the renal medulla of cirrhotic rats. Glomerular filtration rate decreased in cirrhotic rats but was not altered after bosentan treatment in cirrhotic and control rats. Bosentan decreased sodium excretion in both cirrhotic and control rats to a similar extent, whereas water excretion was reduced by bosentan only in cirrhotic rats. We therefore suggest that the upregulation of medullary ETB in cirrhotic rats is involved int he regulation of water excretion in rats with CCl4-induced cirrhosis.

Animals↗
PubMed1994

[A cytofluorimetric study of the glycogen content and of the enzymatic activity of its metabolism in human and animal hepatocytes in liver cirrhosis and during rehabilitation].

Reversibility of hepatocyte functional activity is shown by cytofluorometric and microbiochemical methods in human and rat liver during postcirrhosis rehabilitation. Contents of the total glycogen and its fractions in liver cells were defined on smears of isolated hepatocytes obtained from the live puncture liver biopsies. A double increase of glycogen level is shown, in average, in hepatocytes during experimental liver cirrhosis in rats. At the same time, a relative content of the hard soluble fraction of glycogen increases by 5-8 times. The glycogen level falls to reach the norm already within one month after shutting off the pathogenic influence. However, in some animals after 6 months this level becomes even lower than the normal one. Again, the ratio between the hard soluble fraction and light one remains. In men with cirrhosis glycogenosis of hepatocytes can be expressed in greater degree (increase by 4-5 times): it depends on the illness heaviness. Further changes in glycogen content depend on the pathological process development. Under experimental cirrhosis the activity of glucose-6-phosphatase decreases by 4.3 times. Within one month after stopping the pathogenic influence the activity of this enzyme increases by 3-4 times, but later, in 6 months, it decreases to reach 55-65% of the norm. No actual changes were observed in the activities of other enzymes.

Adult↗
PubMedDate not supplied

[Plasma kallikrein clearance by the liver in experimental cirrhosis].

AIM: To study the hepatic clearance of a glycoprotein (rat plasma kallikrein) by the liver of rats with experimental decompensated cirrhosis. MATERIAL AND METHODS: Cirrhosis was induced by intragastrically administration of carbon tetrachloride 520 mg/kg/week, during 16-19 weeks. After this period, each liver was isolated, exsanguinated and perfused at 37 degrees C with 10nM rat plasma kallikrein (RPK). RESULTS: 58% of the animals died during the treatment and the remaining developed prostration, ascites, jaundice and bleeding; at the end of the treatment period serum aminotransferases were not altered and serum albumin decreased. The liver histology showed cirrhosis. RPK clearance rate of the cirrhosis group (5.4 +/- 0.9 pmol/g liver/10 min) was significantly lower (p < 0.05) than that of the control group (13.5 +/- 2.7 pmol/g liver/10 min). CONCLUSION: The development of cirrhosis is associated with a decreased hepatic clearance of a glycoprotein which endocytosis is mediated by a receptor.

Age Factors↗
PubMed1990

Collagenase of hepatocytes and sinusoidal liver cells in the reversibility of experimental cirrhosis of the liver.

In order to explore the cellular source(s) and the behaviour of the collagenolytic activity previously described in rat liver homogenates, in the reversibility of experimental cirrhosis of the liver, enriched suspensions of hepatocytes and of sinusoidal liver cells were obtained by a procedure which employs low EDTA concentrations and no bacterial collagenase. Cell suspensions were prepared from three different groups of animals: 1) normal controls, 2) rats with CCl4-induced cirrhosis of the liver, and 3) rats with swine serum-induced cirrhosis of the liver. Animals were sacrificed in each group upon completion of treatment and also after 3, 6 and 12 months. In each liver wet weight and collagen concentration were determined, and collagenolytic activity of both enriched cell suspensions was measured separately. In addition, histological studies of liver tissue and ultrastructural examination of cell suspensions were performed by standard procedures. Enriched suspensions of both normal hepatocytes and sinusoidal liver cells display Ca2(+)-dependent collagenolytic activities. Both cell suspensions obtained from each of the two types of cirrhotic livers show normal or slightly increased average levels of collagenase activity at the time of treatment discontinuation, when average liver collagen content ranges from 6 to 10-fold over normal, suggesting that the normal collagenase/collagen ratio is disturbed and that collagenolytic activity is deeply decreased in relation to the actual liver collagen load.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Isolation and characterization of parenchymal cells from experimentally induced macronodular rat liver cirrhosis.

Hepatocytes were isolated from thioacetamide (TAA)-induced macronodular cirrhotic rat livers by a collagenase perfusion method. In the content of cellular metabolites, fatty acid uptake and lipid secretion there were no substantial differences compared with cells isolated from micronodular cirrhosis described previously. In contrast to isolated hepatocytes from normal livers those from macronodular cirrhosis had a lowered cellular content of triglycerides, phospholipids and cholesterol but not of cholesterol esters and free fatty acids. In macronodular cirrhosis hepatocytes of hypertrophic type, rich in cell organelles, can be distinguished ultrastructurally from those with signs of atrophy and degeneration. Immediately after isolation many hepatocytes isolated from macronodular cirrhosis showed plasma membrane blebbing. Whereas the blebbing was without recognizable effects on the fine structure of the isolated hepatocytes of the hypertrophic type, in the more atrophic ones some mitochondria were swollen. In addition, morphological analysis of the crude and purified suspensions revealed a partial selection of the hypertrophic cells during the isolation procedure, presumably due to a more labile state of those cells which showed signs of atrophy and degeneration. When stabilized in the suspension medium, however, the hepatocytes maintained complex metabolic functions for at least 2 h. Thus, the method described allows the isolation of parenchymal cells from TAA-induced macronodular cirrhotic livers for studying ultrastructural and biochemical alterations in hyperregenerative experimental liver cirrhosis.

Animals↗
PubMed1981

The effect of portocaval shunt on bile flow and maximal biliary excretion of bromsulfophthalein sodium (BSP) in rats with thioacetamide induced liver cirrhosis.

Thioacetamide (TAA) causes experimental liver cirrhosis in rats. TAA was administered (50 mg per kg body weight i.p. daily) to sham-operated and shunted rats for eight weeks. Then in pentobarbital anesthesia, bile flow and the maximal biliary excretion (Tm) of BSP were measured using constant infusion technique. Compared to the controls, BSP Tm values decreased significantly in cirrhotic rats. The change results from the lower concentration of dye. In cirrhotic animals the liver cannot excrete the dye per net fluid volume as efficiently, as in the controls. In animals having portocaval shunts and liver cirrhosis, a further decrease of dye excretion can be observed, indicating that the operation has some influence on the canalicular excretion of certain organic anions.

Acetamides↗