Chronic liver injury alters basal and stimulated nitric oxide production and 3H-thymidine incorporation in cultured sinusoidal endothelial cells from rats.

Background/aim: Under pathological conditions the nitric oxide synthase (NOS)-mediated nitric oxide production of sinusoidal endothelial cells might be altered. Therefore, studies were performed to evaluate the nitrite formation by cultured sinusoidal endothelial cells from rat livers chronically injured by thioacetamide and the effect of endogenously or exogenously generated nitric oxide on their proliferative activity.

Methods: Basal and stimulated nitrite formation, expression of NOS and DNA synthesis were examined in sinusoidal endothelial cells isolated and cultivated from livers with incipient or advanced chemically-induced cirrhosis.

Expression of tenascin, fibronectin, and laminin in rat liver fibrogenesis--a comparative immunohistochemical study with two models of liver injury.

The aim of this study was to follow semiquantitatively by immunohistochemical means the alterations of the expression of the hepatic glycoproteins tenascin, fibronectin, and laminin in two different models of chronic liver injury, i.e. thioacetamide-induced liver cirrhosis and fibrosis after bile duct ligation.

Differential effects of exogenous and endogenously generated H2O2 on phagocytic activity and glucose release of normal and cirrhotic livers.

Background/aims: Reactive oxygen species play an essential role in necro-inflammatory processes. Therefore, the aim of the present studies was to investigate the effect of exogenous and endogenously produced H2O2 on the phagocytic capacity and glucose release of perfused cirrhotic rat livers in comparison with that on the controls.

Methods: Complete septal cirrhosis was achieved by oral treatment of rats with thioacetamide for 6 months.

Histological and biochemical changes induced by total bile duct ligation in the rat.

The aim of the present investigation was to assess in a correlated biochemical and morphological study the dynamics of fibrogenesis after bile duct ligation and to compare the time course of alterations with those occurring in thioacetamide induced liver fibrosis. The data show that, after bile duct obstruction, the deposition of connective tissue elements and formation of ductular proliferates rapidly set in. The index of fibroplasia correlated well with the changes of the OH-proline concentration of the liver.

Macrophages from rat livers with micronodular and macronodular cirrhosis differ with respect to mediator release and DNA-synthesis.

Background/aims: Liver macrophages play an essential role in necro-inflammatory liver damage which leads to fibrosis and cirrhosis. The aim of the present study was to compare the mediator release and the DNA synthesis of macrophages at an early and at a later stage of liver cirrhosis induced by thioacetamide.

Methods: Liver macrophages were isolated by an enzymic digestion method, followed by elutriation.

Oxygen radical formation, proliferative activity and phagocytic capacity of cultivated macrophages from cirrhotic rat livers.

A method to isolate and cultivate macrophages from Macronodular-cirrhotic rat livers was developed in order to characterize them biochemically, by comparing various functional parameters in macrophage cell cultures from controls and cirrhotic livers. Cells were prepared from female Wistar rats, made cirrhotic by treatment with thioacetamide, by means of a pronase-collagenase digestion method followed by a nycodenz gradient and elutriation. The yield of macrophages was 8.

Phagocytic function and metabolite production in thioacetamide-induced liver cirrhosis: a comparative study in perfused livers and cultured Kupffer cells.

Background/aims: The aim of the study presented here was to evaluate the basal and stimulated phagocytic activities and the metabolite production of isolated perfused livers, and also the phagocytic capacity of cultured Kupffer cells from rats with macronodular cirrhosis.

Methods: Rats were made cirrhotic by oral administration of thioacetamide. The phagocytic activity was assessed by the rate of removal of colloidal carbon.

Metabolism of leukotrienes is impaired in hepatocytes from rats with thioacetamide-induced liver cirrhosis.

It is likely that the hepatocellular metabolism of potent mediators of inflammation is impaired in chronic liver injury. Therefore, in this study the degradation of the leukotrienes LTC4, LTE4 and LTB4 was investigated in isolated liver parenchymal cells (LPC) from rats with thioacetamide-induced macronodular liver cirrhosis or after bile duct ligation. The degradation of LTE4 as well as the formation of N-acetyl-LTE4 was significantly delayed in LPC from macronodular cirrhotic rats but not in those from bile duct-ligated rats.

Ontogenetic changes in hepatic glutathione system (synthesis, catabolism, export) of male Uje:WIST rats.

The age-courses of concentrations of reduced (GSH) and oxidized (GSSG) glutathione, of GSH synthesizing enzyme activities, of glutathione S-transferase (GST), of GSSG-reductase (GR) and of biliary GSH and GSSG export were measured in livers from male Uje:WIST rats. Additionally, the age-courses of plasma GSH and GSSG concentrations were investigated. The hepatic level of GSH showed a biphasic pattern with a first maximum immediately after birth and a small second peak at the 50th day of life.