Lipopolysaccharide treatment of rats alters antigen expression and oxidative metabolism in hepatic macrophages and endothelial cells

Thomas W. Mc Closkey, Jeanine A. Todaro, Debra L. Laskin – 1 July 1992 – Endothelial cells and macrophages are located within the hepatic sinusoids. These two cell types play an important role in the clearance of bacterially derived lipopolysaccharide from the portal circulation. Our laboratory has previously demonstrated that treatment of rats with lipopolysaccharide results in the accumulation of macrophages in the liver that display properties of activated mononuclear phagocytes. This study was designed to analyze the effects of lipopolysaccharide on hepatic endothelial cells.

Ethinylestradiol increases volume and decreases sinusoidal membrane surface in the rat liver: A stereological analysis

Beat Hornstein, Lukas Stammler, Leonardo Bianchi, Lukas Landmann – 1 July 1992 – Structural alterations of liver parenchyma caused by ethinylestradiol, a synthetic estrogen known to induce cholestasis and to act as a tumor promoter factor, were investigated. Male rats treated with 17α‐ethinylestradiol (5 mg/kg body weight for 5 days) were compared with controls (n = 5 each). After perfusion fixation and systematic random sampling, paraffin sections, semithin sections and thin sections were examined observing standard stereological techniques.

Long‐term follow‐up of patients with chronic hepatitis C treated with α‐interferon

Michiko Shindo, Adrian M. di Bisceglie, Jay H. Hoofnagle – 1 June 1992 – We reanalyzed the results of a pilot study of recombinant α‐interferon therapy for chronic non‐A, non‐B hepatitis in light of the recent discovery of the hepatitis C virus and the development of diagnostic assays for this agent. Stored serum samples from 10 patients treated between 1984 and 1986 were tested for antibody to hepatitis C virus and hepatitis C virus RNA before, during and after therapy.

Effects of vasopressor agents and epoprostenol on systemic hemodynamics and oxygen transport in fulminant hepatic failure

Julia A. Wendon, Phillip M. Harrison, Richard Keays, Alexander E. Gimsson, Graeme J. M. Alexander, Roger Williams – 1 June 1992 – Hypotension is a serious complication in patients with fulminant hepatic failure, because it is associated with tissue hypoxia and a further compromise to end‐organ function. In this study we investigated the effects of epinephrine and norepinephrine on hemodynamics and oxygen transport variables in 30 patients with fulminant hepatic failure. All had a mean arterial pressure of less than 60 mm Hg, despite adequate intravascular filling pressures.

Endocrine mechanisms for the formation of sex‐related differences in hepatic estrogen receptor content and their significance for the realization of an estrogen effect on angiotensinogen blood level in rats

Lidia L. Ignatenko, Guranda D. Mataradze, Victor B. Rozen – 1 June 1992 – The use of a modified, adequate method of quantification of estrogen receptors has permitted us to prove the existence of sex‐specific peculiarities in rat liver estrogen reception and their significance for the realization of sex‐dependent changes in angiotensinogen plasma level after estrogenization. Endocrine mechanisms for the formation of sex‐related differences in hepatic estrogen receptor content in rats were investigated in detail.

Inhibition of superoxide and nitric oxide release and protection from reoxygenation injury by ebselen in rat kupffer cells

Ji‐Feng Wang, Pavel Komarov, Helmut Sies, Herbert de Groot – 1 June 1992 – Luminol chemiluminescence in phorbolesteractivated cultured rat liver Kupffer cells was strongly inhibited by the selenoorganic compound ebselen (IC50 = 2 μmol/L). Ebselen (2‐phenyl‐1,2‐benzisoselenazol‐3[2H]one) also diminished reduction of ferricytochrome c (IC50 = 10μmol/L), indicating a suppression of superoxide anion formation.

What are the intracellular signals for agonist‐activated calcium entry into hepatocytes?

M. Sawkat Anwer – 1 June 1992 – The Ca2+ signal observed in individual fura‐2‐loaded hepatocytes stimulated with the α1‐adrenergic agonist phenylephrine consisted of a variable latency period, a rapid biphasic increase in the cytosolic free Ca2+, followed by a period of maintained elevated cytosolic Ca2+ (plateau phase) that depended on the continued presence of both agonist and external Ca2+, Microinjection of guanosine‐5′‐O‐(3‐thiophosphate) elicited a Ca2+ transient with the same basic features.

Absence of hepatitis B virus precore mutants in patients with chronic hepatitis B responding to interferon‐α

Jianye Xu, David Brown, Tim Harrison, Yue Lin, Geoffrey Dusheiko – 1 June 1992 – Precore defective HBV mutants may gradually prevail because of immune selection and explain spontaneous seroconversion from HBeAg to anti‐HBe in HBV carriers. We have analyzed whether the presence of precore HBV mutants is a determinant of responsiveness to interferon‐α therapy. Fifteen carriers (nine responders and six nonresponders)who were treated with interferon‐α were examined. Serum samples were collected before and after therapy.

Defective biliary excretion of epinephrine metabolites in mutant (TR−) rats: Relation to the pathogenesis of black liver in the dubin‐johnson syndrome and corriedale sheep with an analogous excretory defect

Tsuneo Kitamura, Joseph Alroy, Zenaida Gatmaitan, Masayasu Inoue, Takashi Mikami, Peter Jansen, Irwin M. Arias – 1 June 1992 – Dubin‐Johnson patients, mutant Corriedale sheep and TR− and EHBR mutant rats have recessively inherited defective bile canalicular secretion of many nonbile acid organic anions. The human and ovine mutants have black livers and lysosomal pigment accumulation. The livers in TR− and EHBR mutant rats are not black, and sparse lysosomal pigment accumulation is seen.

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