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Results for “LIVER CIRRHOSIS, EXPERIMENTAL”

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At least 109 records · Page 6Linked to original sources
PubMed1995

[Perisinusoidal stellate cells in a model of experimental liver cirrhosis].

The association of the common bile duct (CBD) ligation followed by CCl4 and progesterone treatment leads to liver cirrhosis in rats in 28 days. The resulting cirrhosis shows mixed aspects: it starts as biliary cirrhosis and goes on to nodular and periportal pseudolobular form of cirrhosis. Because Ito cells are the main source of extracellular matrix components, changing their phenotype from quiescent Ito cells to myofibroblast like cells, the purpose of this study was to evaluate the behaviour of Ito cells by the immunohistochemistry technique of desmin and alpha-SM-actin after these treatments. After CBD ligation alone, positive Ito cells for desmin remarkably proliferate around adenomateous areas; after treatment with CCl4 alone desmin positive stellate cells are more numerous. Desmin positive Ito cells in CBD ligation and CCl4 treatment were even larger than those of the previous lots. Significant differences were not observed after progesterone and for the alpha-SM-actin positive cells.

Animals↗
PubMedDate not supplied

[Metabolism of the basic component of connective tissue at various stages of developing experimental liver cirrhosis].

A system of GAG-hydrolase was studied in liver tissue and blood plasma during development of CCl4-produced cirrhosis of liver tissue in series of experiments involving 400 adult rat males. Dissimilar pathways of the matrix formation, related to dynamics of the GAG-hydrolases activity, were detected within various steps of the chronic CCL4-produced liver tissue impairments in these rats. Alterations in the enzymatic activity were stable and regular in each series of the experiment and correlated with dynamics of the adaptation-compensatory responses.

Animals↗
PubMed1993

[Changes in the hemato-encephalic barrier in experimental liver cirrhosis].

Experiments on 30 Wistar female rats with tetrachloromethane-induced cirrhosis of the liver revealed structural changes in the hematoencephalic barrier presenting as peri- and endocapillary changes and changes in vascular peduncles of astrocytes shown by light and electron microscopy. Hematoencephalic barrier destabilization is conducive to penetration of cerebrotoxins and other metabolic toxins, this explaining the development of hepatic encephalopathy.

Animals↗
PubMed1993

Zinc supplementation in experimental liver cirrhosis: a morphological, structural and ultrastructural study.

Zinc treatment in liver cirrhosis is known to prevent a number of clinical symptoms. Previous studies have also indicated that Zn has a protective effect on the development of the clinical, biochemical and morphological manifestations of hepatic injury if administered simultaneously with the noxious agent. In this study, the protective effects of zinc treatment against the development of liver cirrhosis have been tested in cirrhotic rats treated by intragastric administration of CCl4. The development of morphological lesions has been investigated by means of standardized and comparable techniques, LM, TEM, SEM, microvascular casts and measurements of liver collagen content by colorimetric determination in paraffin embedded sections. LM and EM observations showed typical morphological features of cirrhosis in all CCl4 treated rats. In the same group of animals, the microvascular casts showed the development of the typical 'perinodular' branching and the various anastomoses of pre and post-sinusoidal vessels. Colorimetric evaluation has shown a significant increase in collagen content after CCl4 treatment. Qualitative and quantitative data of livers of CCl4 treated rats supplemented or not with zinc were significantly similar. In conclusion, zinc treatment influences biochemical parameters, but not the morphology of liver cirrhosis.

Animals↗
PubMed1987

Arteriovenous shunting in experimental liver cirrhosis in rats.

The extent of systemic arteriovenous shunting (arteriovenous anastomotic blood flow) was assessed in rats with experimental liver cirrhosis and control rats by injecting 15 micron microspheres into the left ventricle and measuring the percentage of injected spheres trapped in the pulmonary circulation. Cirrhotic rats with body temperature maintained at 38 degrees C were found to have increased trapping of microspheres in the pulmonary bed when compared with control rats studied under similar conditions (8.2% +/- 2.2% vs. 3.6% +/- 0.8%, P less than 0.05). The extent of arteriovenous shunting was also measured in control rats maintained at various body temperatures (34 degrees to 40 degrees C) with and without prior alpha-adrenergic blockade with phenoxybenzamine (0.1 mg/kg). Both body warming and alpha-adrenergic blockade independently increased the extent of arteriovenous shunting. In cirrhotic rats, body warming also increased shunting. However, in contrast to findings in control rats, alpha-adrenergic blockade did not further increase shunting in cirrhotic rats warmed to 40 degrees C. Moreover, the degree of shunting after combined body warming and alpha-adrenergic blockade was similar in cirrhotic and control rats. Our results indicate that increased peripheral arteriovenous shunting occurs in this model of experimental cirrhosis, and that the increased shunting may be related to altered physiologic regulation of arteriovenous anastomotic blood flow.

Adrenergic alpha-Antagonists↗