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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Content of individual phospholipids, gangliosides and lipid peroxidation were studied in liver tissue homogenates of rats with hepatitis caused by CCl4 or heliotrine. In all the cases studied the rate of lipid peroxidation was distinctly increased, while content of sphingomyelin was decreased and that of phosphatic acid--increased; concentration of some gangliosides was altered. Activation of lipid peroxidation appears to induce the enzymatic systems involved in degradation of phospholipids and gangliosides in liver tissue of rats with toxic hepatitis.
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PMID:[Change in lipid peroxidation processes and level of individual gangliosides and phospholipids in the liver of rats with toxic experimental hepatitis]. 175 88

Specific binding of 125I-labeled human recombinant HGF to the primary cultured rat hepatocytes or liver plasma membranes was observed to be temperature- and time-dependent. Scatchard analysis indicated the presence of a single class of high affinity receptors with a dissociation constant (Kd) of 24-32 pM, a value in good accord with half maximum dose for HGF activity and a receptor density of about 500-600 sites/cell. Affinity cross-linking of the receptor with 125I-HGF revealed the HGF receptor in rat liver membranes to be a polypeptide of Mr approximately 220,000. After partial hepatectomy, specific binding of 125I-HGF to the membranes of residual livers decreased by 60-70% between 3 and 6 h, and was scanty at 12 h after hepatectomy. After one week, the binding was recovered to the 1.7 fold level in the untreated rat liver. This rapid down-regulation of HGF receptors was also observed in plasma membranes of rat livers in the presence of hepatitis induced by CCl4. We propose that HGF which can be immediately supplied to the liver after hepatic injury will function as a trigger for regeneration of this organ.
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PMID:Identification and change in the receptor for hepatocyte growth factor in rat liver after partial hepatectomy or induced hepatitis. 182 59

Hepatocyte Growth Factor (HGF), which is a most potent growth factor for primary cultured hepatocytes, may act as a trigger for liver regeneration. After 70% of the rat liver was removed, HGF activity in the remnant liver began to increase within 24 h. In parallel with the activity, the HGF mRNA level in the remnant liver increased at 12 h after the operation and reached a maximum at 24 h. Increases in HGF activity and in the mRNA level were much lower and later than those in the liver of rats with hepatitis induced with CCl4. However, the first increase in HGF activity in the plasma of hepatectomized rats was noted 3 h after the resection, that is much earlier than the initial DNA synthesis in the remnant liver. Thus, while HGF production was induced in the remnant liver during regeneration after partial hepatectomy, the initial trigger may not be the liver-derived HGF, rather, it may be HGF derived from extrahepatic organs, via blood circulation.
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PMID:Possible endocrine control by hepatocyte growth factor of liver regeneration after partial hepatectomy. 182 41

In order to estimate contact interactions and deformity of the surface of hepatocytes at a toxic hepatitis, produced by means of carbon tetrachloride, a morphometric analysis of ultrastructures of the contacts and retractions of the surface of hepatocytes, formed at an increased intraorganic pressure has been performed. Carbon tetrachloride produces decrease in adhesive interactions of the cellular surfaces in the area of simple connections, decrease in amount of desmosomes and results in increasing deformity of the surface of hepatocytes. These data support that there exists a universal reaction of the intercellular contacts to a damaging action.
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PMID:[Status of cell surface of hepatocytes after exposure to carbon tetrachloride]. 209 59

A hepatoprotector of phospholipid nature eplir extracted from silt mud was shown to prevent like essentiale in CCl4-hepatitis in rats the development of the liver parenchyma necroses, to promote the maintenance of the normal activity of enzymes in hepatocytes, to stabilize lysosomes, to stimulate the antitoxic and excretory functions of the liver, to reduce hyperfermentemia. The mechanism of action of eplir is determined by the antioxidant properties, a decrease of lysophosphatide formation and the inclusion of phosphatidylcholine in membranes.
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PMID:[The effect of eplir on an experimental toxic lesion of the liver]. 225 48

Drugs obtained from the roots and leaves of plantation ginseng and ginseng root tissue culture displayed a high antidiabetic and hepatoprotective activity in experiments on mice and rats. In alloxan diabetes these adaptogenic phyto-agents prevented alloxan-induced activation of processes of lipid peroxidation in the pancreas and demonstrated definite insulinogenic properties: they increased the basal content of insulin in blood and the glucose-dependent secretion of this hormone. In CCl4 acute toxic hepatitis the studies ginseng drugs reduced the disorders of hepatic detoxification and glycogen-synthesizing functions.
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PMID:[Efficacy of ginseng drugs in experimental insulin-dependent diabetes and toxic hepatitis]. 229 65

The effect of polyphytochol representing a combination of vegetable agents was studied on models of acute toxic hepatitis caused by CCl4 and cholecystitis. The efficiency of the drug in pathology of the hepatobiliary system was shown: it decreases cholestasis acting as a choleretic and bile-secreting drug, acts on the main pathogenetic links in hepatitis, exerts a marked membrane-stabilizing effect, influences favourably the processes of synthesis in the liver.
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PMID:[The characteristics of the action of polyphytochol on the course of experimental hepatitis and cholecystitis]. 236 54

Administration of galbanic acid isolated from the roots of Ferula kopetdaghensis Eug. Kor. to rats orally in a dose of 50 mg/kg was found to improve the course of toxic hepatitis induced by fourfold subcutaneous injections of a 50% oil solution of CCl4. Galbanic acid produced much more earlier than in control normalization of the activity of the enzymes alanine- and aspartataminotransferase in blood serum, increased glycogen content and improved the parameters of the redox potential of lactic acid-pyruvic acid system in the liver. Galbanic acid exerted the antioxidant effect. In the animals with a developed hepatitis receiving galbanic acid there was a more rapid restoration of intensity of bile secretion, synthesis of bile acids and bilirubin, cholesterol excretion as compared with control.
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PMID:[The effect of galbanic acid on the course of experimental hepatitis]. 236 53

Two physiologically based pharmacokinetic models A and B incorporating enterohepatic recycling, which succeeded previously in predicting the disposition of glycyrrhizin (GLZ) in normal rats and subjects, were applied to predict GLZ disposition in plasma and tissues of chronically CCl4-intoxicated rats, and serum of humans with hepatitis after i.v. dosing. The prediction by model A with the direct excretion of GLZ from liver into gut lumen gave fairly good agreement with the observed time courses of GLZ concentrations in blood and tissues in the intoxicated rats. The human serum disposition was predicted by model B, to which was added a gallbladder for the excretion from liver into gut lumen to model A by assuming continuous delaying transfer from the gallbladder. An attempt to predict the serum dispositions in five human subjects by considering individual differences in serum free fraction, biliary excretion ratio, and intestinal absorption clearance was successful in model B. Thus, scale-up of the disposition kinetics of GLZ from rat to man with liver failure was successful.
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PMID:Prediction of glycyrrhizin disposition in rat and man with liver failure by a physiologically based pharmacokinetic model. 238 51

Pharmacokinetic analysis of lidocaine (Lid) and its metabolites, monoethylglycinexylidide (MEGX) and glycinexylidide (GX), was performed in a dog bearing carbon tetrachloride (CCl4, 0.75 ml/kg ip)-induced acute hepatitis. Following pentobarbital sodium (25 mg/kg iv) anesthesia, lidocaine hydrochloride (2.5 mg/kg iv) was given and arterial blood was drawn 2, 5, 10, 15, 30, 45, 60, 90, and 120 min after administration. Lid and its metabolites in plasma were extracted with chloroform-hexane-isopropanol (60 : 30 : 10), and organic layer was dried down at 50 degrees C under N2. The residue was dissolved in 50mM phosphoric acid and subjected to HPLC analysis. 4-compartment model was introduced to analyze pharmacokinetic parameters, and which gave the most reasonable fit with actual results. Control experiment was carried out using identical dog with acute hepatitis. The following results were given: 1) Elimination of Lid was slightly depressed, but T1/2 was not altered. Plasma level of Lid was kept higher. 2) As for MEGX, the formation was depressed, and upto 23 min after Lid administration, MEGX concentration in the dog with acute hepatitis was lower than that of control, but after 23 min it was vice versa. 3) As for GX, the formation was depressed, but the elimination was not affected. In the dog with CCl4-induced hepatitis, metabolism of Lid was suppressed, and which resulted in maintaining a relatively higher levels of Lid and MEGX concentration in plasma. These results suggested that care should be taken to avoid acute poisoning with Lid especially in patients with acute hepatitis.
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PMID:[Pharmacokinetics of lidocaine and its metabolites in dog. Comparison between normal and CCl4-induced hepatic lesion]. 248 93


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