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Query: UMLS:C0239946 (liver fibrosis)
 8,268 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify the effect of the pathological state of the liver on ultrasonic attenuation, we produced two experimental rabbit models. The influence of fat on ultrasonic attenuation was examined using a fatty liver model without liver fibrosis, and that of fibrosis on attenuation using a liver fibrosis model without fatty infiltration. Ultrasonic data were obtained in vivo directly from the liver, and an acoustic attenuation coefficient slope was obtained by the spectral difference method. Tissue components of the liver, namely the total lipid, hydroxyproline and water contents, were measured precisely by quantitative methods. We revealed that ultrasonic attenuation depends mainly on fatty infiltration of the liver and to a lesser extent on fibrosis, but not on the water content.
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PMID:Dependence of ultrasonic attenuation of liver on pathologic fat and fibrosis: examination with experimental fatty liver and liver fibrosis models. 144 Sep 87

Adding less than 0.5% w/w of culture material of strain MRC 826 of the fungus Fusarium moniliforme to a carbohydrate diet low in fat resulted in an atherogenic plasma lipid profile in a non-human primate. Simultaneously increased plasma fibrinogen and activity of blood coagulation factor VII could enhance atherogenesis. This unique potential for promotion of atherosclerosis was probably secondary to chronic hepatotoxicity as indicated by liver fibrosis and elevated cholesterol, albumin and the enzymes AST, ALT, LD, GGT and ALP in serum. The cholesterol and enzymes responded in proportion to the calculated doses of fumonisin mycotoxins in the F. moniliforme MRC 826 cultures. Fumonisins are water soluble and heat stable. Thrombotic, hepatotoxic, carcinogenic and cerebral effects of MRC 826 culture material and fumonisins are well known in non-primates. The estimated fumonisin concentrations tested fall within a range due to natural contamination of human foods. The results suggest that all maize grain products should be analysed for fumonisins.
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PMID:Atherogenic effects in a non-human primate of Fusarium moniliforme cultures added to a carbohydrate diet. 163 55

The organ distribution of 3H-endotoxin was investigated in rats with CCl4-induced liver injury. Wistar male rats were given water containing phenobarbital (Controls), or were treated with water containing phenobarbital and CCl4 inhalation. Rats inhaling CCl4 for 6 weeks developed liver fibrosis (Group LF), while those inhaling it for 10 weeks developed liver cirrhosis (Group LC). Animals were killed and examined 24 hours after an intravenous injection of 3H-endotoxin (12,000 CPM/l g body weight). Compared with the control rats, the measured amount of 3H-endotoxin per unit weight of spleen, lungs, and blood increased, while that of the liver significantly decreased in the rats of groups LF and LC. These results suggest that endotoxemia may be enhanced by a diminished uptake of endotoxin by the liver in liver fibrosis and liver cirrhosis.
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PMID:Organ distribution of 3H-endotoxin in rats with liver fibrosis and rats with liver cirrhosis. 275 63

Male F-344 rats were treated for 10 weeks either with CCl4 (0.2 ml/kg, per os, twice a week) or with CCl4 (same as above) and phenobarbital (0.2 g/l in drinking water). Liver fibrosis and cirrhosis developed in both treated groups, and was confirmed histologically. Cirrhosis was more frequent after the CCl4 + phenobarbital treatment. The collagen content of the liver, measured by morphometry and biochemically, was significantly higher in the animals of the group treated with CCl4 + phenobarbital than in the animals treated only with CCl4. Specially altered fat-storing cells (Ito cells) were found in the periportal and septal fibrotic areas in direct proportion to the amount of fibrosis and cirrhosis. They were identified as altered fat-storing cells by their desmin content and Vitamin A storing capability. This study demonstrated that these cells were enlarged and contained neutral fat, lipofuscin and PAS-positive material. The potential role of GAG-containing FSC in fibrogenesis is discussed.
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PMID:Glycosaminoglycan containing fat-storing cells in hepatic fibrogenesis. 315 42

During the development of liver fibrosis in rats by an individual dose-titrated CCl4 administration, hepatic proton spin-lattice relaxation time (T1) has been measured in vivo every 2 weeks for 8 weeks. Liver content of collagen, triglycerides and water has been measured biochemically in biopsy material. After 4 weeks of CCl4 treatment, T1 increased significantly and remained at the same level, whereas liver collagen reached its maximum at 8 weeks. It is concluded that, under our experimental conditions, increased hepatic T1 represents drug-induced edema and that hepatic T1 is not a reliable noninvasive parameter for developing liver fibrosis in vivo.
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PMID:Is the magnetic resonance imaging proton spin-lattice relaxation time a reliable noninvasive parameter of developing liver fibrosis? 335 2

Acute and chronic liver damage was induced in rats by thioacetamide (TAA). Centrilobular liver cell damage associated with an accumulation of lipid droplets was produced by a single high dose (10 mg TAA/100 g b.m.). Liver fibrosis, micronodular and macronodular liver cirrhosis were induced by chronic TAA treatment (300 ml/l drinking water for 1.5, 3 or 6 months). Acute administration of TAA caused a significant decrease of hepatic phenol red excretion but no compensatory increase of its urinary excretion. In contrast, 24 h after bile duct ligation renal excretion of the dye increased by about 50%. After chronic exposure to TAA for three months hepatic phenol red excretion remained reduced and renal excretion raised significantly. This compensatory increase of urinary excreted phenol red amounts did not occur after 6 months of TAA treatment, probably as a result of additional nephrotoxicity of TAA. Two weeks after cessation of TAA exposure for 3 months, hepatic and renal phenol red excretion returned to normal. Bile flow per animal increased significantly after 3 months of TAA exposure. Apparently this is due to a reduced intrahepatic reabsorption of canalicular bile in TAA-damaged liver.
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PMID:Relation between renal and hepatic excretion of drugs: VII. Hepatic and renal excretion of phenol red in thioacetamide-induced acute and chronic liver damage. 338 66

Periportal fibrosis and portal hypertension were induced by periodic retrograde biliary injections of sesame oil for two to three months in 12 cholecystectomized dogs equipped with Thomas cannulas. Stable portal hypertension between 18 and 24 cm of water occurred in four of 12 dogs (baseline: 10.4 +/- 0.5 cm of water); the remaining eight dogs required continuous biliary oil injections to maintain the portal pressure in that range. Portosystemic venous collaterals were first seen three weeks after the initial biliary oil injection and were extensively developed after two months. Hepatopetal portal blood flow decreased 61 +/- 5% during the first six months, with the greatest decrease of 32 +/- 4% occurring in the first month. Hepatic arterial flow did not change in the first month and then began to rise slowly to peak at nine months at 170 +/- 32% of its baseline value. The greatest increase in hepatic arterial flow was found between the sixth and ninth month when the portal flow no longer changed significantly. Hepatic fibrosis originating from the portal triads and around extravasated oil droplets appeared to progress slowly during the entire observation period. Animals with advanced hepatic fibrosis remained in satisfactory general health with liver enzymes usually remaining in the high normal to low pathologic range, allowing extensive follow-up examinations at regular intervals.
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PMID:Angiographic, hemodynamic, and histologic evaluation of portal hypertension and periportal fibrosis induced in the dog by retrograde biliary injections of sesame oil. 373 82

Sake or bourbon (8g ethanol/kg body weight) was intragastrically administered to rats for 12 days. An equal dose of ethanol in water or an isocaloric glucose solution was administered to control groups. Food was withheld, but water freely provided. Neither mortality nor liver and body weights were different between the alcohol-treated groups. Glutamic oxaloacetic transaminase and glutamic pyruvic transaminase were more elevated in the sake group than in the other groups. Additionally, liver fibrosis was more pronounced, and vacuole formation or steatosis was less in this group. These results suggest that sake is more fibrogenic. Some components other than ethanol, such as long-alkyl chain alcohols, may have been responsible for the differential histopathology.
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PMID:Effects of sake and bourbon on liver histopathology and function in rats. 652 45

Rats treated with carbon tetrachloride (CCl4, twice weekly 0.2 ml/kg p.o.) and a 5% ethanol solution instead of drinking water developed a marked fibrosis and steatosis of the liver within 4 weeks. Fibrosis was evidenced by a 7-fold increase in the hepatic hydroxyproline content and steatosis by a 3-fold increase in the triglyceride content. Exposing these rats to a non-narcotic concentration of halothane (100 ppm) in a closed system the metabolic removal of the anesthetic from the atmosphere of the system was measured. In control rats treated with olive oil and water the elimination half-life for halothane amounted to 0,78 (0,69-0.88) h (confidence limits for p = 0.95). In rats with CCl4-ethanol-induced liver fibrosis and steatosis this elimination half-life was prolonged to 1.24 (1.07-1.41) h indicating an impaired metabolic degradation of halothane in these rats.
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PMID:[Metabolism of halothane in rats with CCl4-alcohol-induced liver fibrosis]. 684 83

1. Subchronic treatment of male and female rats with CCl4 (0.2 ml/kg orally twice weekly) and drinking water containing 5% ethanol for four weeks led to a 20 to 40-fold increase in serum sorbitol dehydrogenase activity and to an augmentation of the liver triglyceride and hydroxyproline contents, indicating steatosis and fibrosis, respectively. Liver fibrosis was less pronounced in females than in male rats. 2. As a consequence of these alterations the hepatic microsomal mixed-function oxidase activity as measured by aminopyrine demethylation was decreased with concomitant loss of cytochrome P-450 in both sexes. Aniline hydroxylation as well as the activity of the NADPH-cytochrome c reductase showed no significant alterations. 3. While the hepatic glutathione content remained unchanged, the cytosolic glutathione S-transferase activities towards both an aryl and an epoxide substrate were markedly decreased following the development of liver fibrosis both in male and female rats.
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PMID:Effect of carbon tetrachloride--alcohol-induced liver fibrosis on microsomal mixed-function oxidases and the cytosolic glutathione-conjugating system in rat liver. 685


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