Inhibition of glutathione synthesis in the liver leads to S‐adenosyl‐L‐methionine synthetase reduction

Fernando Corrales, Pilar Ochoa, Carmen Rivas, Manuel Martin‐Lomas, José M. Mato, Maria A. Pajares – 1 September 1991 – The hepatic levels of glutathione in rats treated with buthionine sulfoximine (4 mmol/kg), an inhibitor of glutathione synthesis, were 72.5% ± 4.9% of those determined in control animals. This decrease in glutathione concentration was prevented by the administration of glutathione monoethyl ester (7.5 mmol/kg). S‐Adenosyl‐L‐methionine‐synthetase activity in the liver of rats treated with buthionine sulfoximine was 39.4% ± 6.5% of that determined in control animals.

Increased expression of intercellular adhesion molecule 1 on bile ducts in primary biliary cirrhosis and primary sclerosing cholangitis

David H. Adams, Stefan G. Hubscher, Jean Shaw, Gerald D. Johnson, Christopher Babbs, Robert Rothlein, James M. Neuberger – 1 September 1991 – It has been suggested that immunological mechanisms involving lymphocyte‐mediated damage are important in the characteristic bile‐duct damage that occurs in primary biliary cirrhosis and primary sclerosing cholangitis.

Export of intracellular HBsAg in chronic hepatitis B virus infection is related to viral replication

Johnson Y. N. Lau, Vincent G. Bain, Susan E. Davies, Graeme J. M. Alexander, Roger Williams – 1 September 1991 – Serum and liver HBsAg bear an inverse relation to each other during the evolution of chronic hepatitis B virus infection and the quantity of HBsAg in tissue rises gradually with time. In this study, intracellular and extracellular levels of HBsAg were measured by radioimmunoassay in primary culture of hepatocytes from 30 patients with chronic hepatitis B virus infection to determine a possible relationship with hepatitis B virus replication.

Protection by 16,16‐dimethyl prostaglandin E2 and dibutyryl cyclic AMP against complement‐mediated hepatic necrosis in rats

Yoichi Kurebayashi, Yuko Honda – 1 September 1991 – 16,16‐Dimethyl prostaglandin E2, a known cytoprotective agent, was examined for its ability to protect the liver against complement‐mediated necrosis induced by an intravenous injection of a monoclonal antibody against a rat liver—specific antigen in rats.

Movement of IgM antibody from blood to bile in rats

Peter G. C. Hansen, Graham D. F. Jackson – 1 September 1991 – The movement from blood to bile of passively injected autologous IgM antibody against horse erythrocytes was studied in rats. Both native and neuraminidase‐treated antibody entered bile intact, with the peak titers for both measured between 60 and 90 min after injection. A small part (0.38%) of the injected dose of native antibody and 1.05% of the asialo‐IgM antibody appeared in bile over 24 hr. These recoveries represented only a small fraction of the activity, which apparently disappeared from serum over the period.

Systemic, splanchnic and renal hemodynamic effects of a dopaminergic dose of dopamine in patients with cirrhosis

Yannick Bacq, Christophe Gaudin, Antoine Hadengue, Dominique Roulot, Alain Braillon, Richard Moreau, Didier Lebrec – 1 September 1991 – The effects of dopamine on kidney function have not been elucidated in patients with cirrhosis. Moreover, although increased portal pressure has been observed with supradopaminergic doses of dopamine in these patients, the splanchnic hemodynamic effects of low doses of dopamine have not been previously studied.

Is intrapulmonary arteriovenous shunting and hypoxemia a contraindication for liver transplantation?

L. Siw Eriksson – 1 September 1991 – A 12‐year‐old boy with Wilson's disease developed exertional dyspnea, cyanosis, and finger clubbing 10 months after diagnosis. The hypoxemia was caused by arteriovenous shunting, demonstrated by radionuclide scanning and pulmonary arteriography. Orthotopic liver transplantation was performed after the development of severe hypoxemia. There was no apparent reversal of the intrapulmonary arteriovenous shunting and he died 10 days posttransplantation of multiple organ failure secondary to hypoxemia.

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