Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors examined the action of D-penicillamine on the ultrastructure of hepatocytes and the condition of the base substance in the rat's liver, with experimental CCl4-cirrhosis. (D-penicillamine was given to these rats during 4 and 6 months). It was discovered that the using of D-penicillamine on the early stages of experiment (until 4 months) reduced the process of the development of the liver cirrhosis. This fact was confirmed by the reducing of the level of base substance in the liver and reducing of the quantity of collagen in the Disse space, as well as by the absence of fibres in the intercellular spaces near sinusoid. When the D-penicillamine was given longer the increasing of the beta-NAG activity with simultaneous severe reducing of the GAG and destruction of hepatocyte's organelles in the experimental rat to the 6 months of experiment were observed. The authors consider that these data are the evidence of the negative effect of the long using of D-penicillamine in the stage of decompensated cirrhosis of the liver.
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PMID:[Effects of D-penicillamine on the ultrastructure of hepatocytes and state of the base substance in the liver of rats with experimental cirrhosis]. 233 8

The distribution of cathepsin D in liver with CCl4 induced cirrhosis and its involution in rats was investigated by ultrastructural cytochemistry. Besides intracellular, it was revealed the extracellular activity of cathepsin D. The reaction product was on collagen fibers near the hepatocytes and connective tissue cells as well as on the hepatocytes microvilli and on the outside part of cellular membrane of connective tissue cells (macrophage, fibroblast, Ito cells). Hence the source of extracellular cathepsin D in liver are the parenchymatous as well as nonparenchymal cell elements. The results testify that under the cirrhosis and its involution, the cathepsin D takes part in intracellular proteolysis and is secreted by hepatocytes and connective tissue cells in the intracellular space; it also takes part in extracellular catabolism of connective tissue.
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PMID:[Intracellular and extracellular activity of cathepsin D in the liver in cirrhosis and its involution]. 233 65

The purpose of this paper is to provide a histopathologic basis for abnormalities in immune-complex clearance in liver disease. Fc receptors in CCl4-induced liver cirrhosis in rats were studied by applying peroxidase-antiperoxidase immunoglobulin G complex as a ligand to the frozen sections. Intravenous injection of bovine serum albumin-antibovine serum albumin complexes or colloidal carbon was combined with histological staining for endogenous peroxidase, fibronectin, laminin, or a lectin, Bandeiraea simplicifolia agglutinin I. In the cirrhotic process, sinusoidal Fc receptors showed a weakened reactivity to the ligand with focal absence, and the length of the Fc receptor-positive portion of the sinusoids in unit area decreased to about 50% of the normal value in the advanced cirrhosis. Fibronectin and the lectin showed the presence of sinusoids where Fc receptors were absent. The endothelium in Fc receptor-negative areas did not take up either immune complexes or carbon, and Kupffer cells were absent in these areas. A disturbed immune-complex metabolism was thus suggested to occur in association with the defect of sinusoidal Fc receptors in liver cirrhosis. These abnormalities appeared to not be directly related to perisinusoidal laminin deposition, i.e., capillarization of the sinusoid.
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PMID:Defect of sinusoidal Fc receptors and immune complex uptake in CCl4-induced liver cirrhosis in rats. 234 26

In order to pinpoint the site causing increased intrahepatic vascular resistance, we observed the relationship between hepatic pathologic changes and free portal pressure (FPP) during the development of CCl4-induced liver cirrhosis of rat. The results suggested that the degeneration necrosis and regeneration of liver cells, and consequent stenosis, or obliteration of sinusoidal spaces caused by the swelling and disarrangement of the liver cell plates led to the occurrence of portal hypertension. The possibility of pre- or post-sinusoidal obstruction was excluded by the manifestation of the pathologic lesions. It is the authors' belief that the exact site of the increased intrahepatic vascular resistance was most likely at the level of hepatic sinusoids. Furthermore, there was certain positive correlation between plasma glucagon concentration and FPP, indicating that glucagon was also involved in the pathogenesis of portal hypertension.
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PMID:[Relation of hepatic pathologic changes and portal venous pressure in the course of cirrhosis in rats]. 237 24

In efforts to understand mechanisms of liver dysfunction in cirrhosis, transcription of specific genes important to liver function has been measured in the rat model of CCl4-induced hepatic fibrosis. The relative transcription rates of albumin, alpha-fetoprotein and pro-alpha 1-collagen genes were studied during development of fibrosis and after fibrosis was established. During the initial phase of CCl4 administration, there was a decrease in albumin transcription associated with increased alpha-fetoprotein transcription, indicative of active liver regeneration. However, later during development of fibrosis, the response pattern of these genes was different, as albumin gene transcription was normal or increased and alpha-fetoprotein gene transcription was no longer increased. Three weeks after completion of CCl4 treatment (fully established cirrhosis), albumin genes responded normally or hypernormally to an acute regenerative stimulus, but the alpha-fetoprotein gene was again not measurably responsive. Pro-alpha 1-collagen gene transcription increased during the entire fibrogenic process and remained elevated after cirrhosis was established. These studies suggest that a switch from albumin to alpha-fetoprotein gene transcription can serve as a marker of liver regenerative capacity, and that this process is altered during and after development of hepatic fibrosis. The fibrogenic process is also associated with elevated transcription of collagen genes.
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PMID:Changes in albumin, alpha-fetoprotein and collagen gene transcription in CCl4-induced hepatic fibrosis. 245 32

We undertook a study to evaluate the correlation between morphometric evaluation and colorimetric determination of hepatic collagen content, and to analyze the variation among animals as well as among lobes of the same liver in hepatic collagen content after CCl4-induced micronodular cirrhosis. The results revealed a significant correlation (r = 0.9458; p less than 0.001) between the morphometric and colorimetric methods of collagen evaluation of liver specimens; both methods also significantly distinguished data obtained from controls and from cirrhotic rats (p less than 0.0005). After induction of micronodular cirrhosis by chronic CCl4 administration, a highly significant variation in hepatic collagen content was observed among animals (p less than 0.0001). By contrast, no significant difference in collagen content was observed (p less than 0.05) among hepatic lobes of a given animal. These results indicate that in this animal model of liver cirrhosis, interpretation of biochemical data would benefit by being related to the severity of the hepatic collagen infiltration of each animal. Our data also show that representative values for total hepatic collagen infiltration can be obtained from a single liver specimen; we suggest, however, that the specimen be taken from a major lobe of the liver and that a sufficiently large number of animals be used to avoid occasional sampling errors.
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PMID:Estimation of collagen content of liver specimens. Variation among animals and among hepatic lobes in cirrhotic rats. 246 35

Carbon tetrachloride was used to induce cirrhosis in 81 Wistar rats. The animals were divided into three groups to receive end-to-side mesocaval shunt (MCS), end-to-side portacaval shunt (PCS) and Sham operation as control, respectively. Dynamic values of blood glucose and hormones for regulating glucose metabolism, SGPT, serum glycine conjugated cholic acid (CCA) and free serum amino acids were determined and compared with those obtained from 10 normal rats. The determinations suggested that the insulin level depended on the severity of hepatocellular damage with hyperglucagonemia after portasystemic shunt, and CCA was markedly elevated in MCS rats after interruption of the enterohepatic circulation. Changes of CCA were also influenced by hyperglucagonemia and poor liver function in PCS rats. Increase in the aromatic amino acids (AAA) level was related to the impaired hepatic function and hyperglucagonemia. However, decrease in the branched-chain amino acids (BCAA) level was not likely in response to the serum insulin level. Therefore, it is concluded that imbalance of serum amino acids has partial relationship with the derangement of glucose metabolic hormones.
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PMID:Metabolic derangement of glucose, bile acid and amino acids after portasystemic shunts in cirrhotic rats. 251 64

Effect of cirrhosis on the wound healing was investigated in the rat. Experimental cirrhosis was induced by oral administration of carbon tetrachloride (CCl4). The number of infiltrating cells in the gastric and abdominal wounds was significantly decreased in the cirrhosis group. And the collagen content, represented as hydroxyproline, was also decreased in the wounds of cirrhotic rats. These decreases were positively correlated to the severity of the cirrhosis. These results indicate that the wound healing was impaired in both the inflammatory and the proliferative phase in the cirrhotic rats. The bursting pressure, which represents the physical strength of the wounds, was also lowered in the cirrhosis group. Correlations were observed among the infiltrating cell number, the collagen content and the bursting pressure respectively. These findings indicate that the damage caused by cirrhosis in the inflammatory phase affects the proliferative phase of wound healing. Administration of fresh plasma increased the number of infiltrating cells and the collagen content in the wounds, and was expected to promote the wound healing.
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PMID:[Experimental study of the wound healing in liver cirrhosis]. 253 39

Reduced hepatic uptake and clearance of macromolecules in liver cirrhosis is due to two major factors: increased diffusional barriers, resulting primarily from the deposition of excessive connective tissue in the space of Disse, and hepatocellular dysfunction, manifested by receptor and/or postreceptor defects. To probe the mechanisms underlying hepatocellular dysfunction in liver cirrhosis, we have investigated receptor-ligand interactions for asialoorosomucoid, insulin and epidermal growth factor in hepatocytes isolated from the livers of rats chronically exposed to phenobarbital and carbon tetrachloride for up to 12 weeks. Viable cells were allowed to attach at 37 degrees C and the high-affinity cell surface binding sites for each ligand were assessed at 4 degrees C in the presence of [125I]-ligand. In parallel incubations, digitonin (0.055%) was added to the binding medium to assess total cellular binding sites. Results demonstrated that chronic treatment of rats with phenobarbital increased hepatocyte asialoorosomucoid surface receptor affinity (p less than 0.05) but had no affect on the number of asialoglycoprotein binding sites. Treatment with CCl4 and phenobarbital significantly reduced the number of surface binding sites for asialoorosomucoid (p less than 0.05) and epidermal growth factor (p less than 0.02), although this treatment had no effect on either the binding affinity or the number of binding sites for insulin. The decrease in cell surface binding sites for asialoorosomucoid and epidermal growth factor was not due to a redistribution of the surface sites to intracellular locations, since the total number of cellular binding sites also was reduced.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alterations in the functional expression of receptors on cirrhotic rat hepatocytes. 253 99

The effects of propranolol on liver functions of healthy rats were studied administering daily doses of 1 mg/kg. Beta receptor blockade has been investigated in carbontetrachloride induced liver cirrhosis. Normal liver functions were unchanged with the exception of an increase in Glucos-6-Phosphatase. The severe cirrhotic injuries were counteracted or moderated when propranolol administration started the same day as CCl4 injection. The amount and function of mixed-function-monooxygenases were normalised. Carbohydrate and protein metabolism impairments were moderated. Serum triglyceride and HDL-cholesterin levels were however uninfluenced. The metabolic properties of propranolol seem to be advantageous in chronic liver impairments.
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PMID:[Beta receptor blockade and liver function]. 254 Jun 15


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