Charles L. H. van Berlo, Anton E. J. M. van de Bogaard, Marion A. H. van der Heijden, Hans M. H. van Eijk, Mieke A. Janssen, May C. F. Bost, Peter B. Soeters – 1 September 1989 – A variable protein‐induced toxicity has been reported in liver disease. The aim of this study was to establish the cause of increased ammonia liberation in the gut after intraluminal bleeding. Therefore, blood was sampled from catheterized piglets [20 ± 0.8 kg (means ± S.E.); n = 10] to determine ammonia, urea and amino acid levels before and 1, 2, 3 and 6 hr after a standard pig meal (750 gm, 12% protein).

Tsunehisa Kawasaki, Frederick J. Carmichael, Gwynne Giles, Victor Saldivia, Yedy Israel, Hector Orrego – 1 September 1989 – The treatment of alcoholic liver disease with propylthiouracil is based on its effect of suppressing the ethanol‐induced increase in hepatic oxygen consumption. It has been postulated that liver necrosis ensues when the increase in oxygen demand by the liver exceeds oxygen delivery to this organ. Data are now presented which show that propylthiouracil also increases portal blood flow in awake, unrestrained rats.

H. Greim, L. Schwarz – 1 August 1989

Isabelle Fourel, Philippe Gripon, Oliver Hantz, Lucyna Cova, Véronique Lambert, Chantal Jacquet, Kyoichi Watanabe, Jack Fox, Christiane Guillouzo, Christian Trepo – 1 August 1989 – Duck cultured hepatocytes from Pekin ducks naturally infected by duck hepatitis B virus can remain functional twice longer if a coculture system with rat liver epithelial cells is used instead of ordinary primary culture.

Serge Erlinger – 1 August 1989

Matthias Goerig, Heinrich Wernze, Burkhard Kommerell, Martin Grün – 1 August 1989 – Metabolites of arachidonic acid have been attributed to severe circulatory, metabolic and hormonal alterations in patients with chronic liver disease. In order to study changes of the tissue‐specific availability of enzymes of eicosanoid synthesis, we used portacavalshunted rats, as this model exhibits many clinical and biochemical similarities to patients suffering from cirrhosis of the liver.

1 August 1989

Sonia M. F. de Morais, Peter G. Wells – 1 August 1989 – Glucuronidation is the major pathway for elimination of acetaminophen, diverting it from the toxifying pathway catalyzed by cytochromes P‐450. A genetic deficiency in bilirubin UDP‐glucuronyl transferase may predispose humans and animals to the toxicity of drugs that are extensively glucuronidated, if other glucuronyl transferase isoenzymes are concurrently deficient. Homozygous and heterozygous Gunn rats are, respectively, severely and moderately deficient in glucuronyl transferase.

Stephen J. Williams, Geoffrey C. Farrell – 1 August 1989 – The present study was performed to establish whether sequential determinations of antipyrine clearance, using a simplified two‐point test, are sensitive and specific indicators of changes in chronic hepatitis B disease activity. Sixteen patients were studied on four or more occasions during 18 to 30 months. Eleven patients were treated with recombinant human α‐interferon (2.5, 5.0 or 10 × 106 per m2, intramuscularly, three times per week, for 24 weeks), and five patients were untreated controls.

Martin Rössle, Jürgen Deckert, E. Anthony Jones – 1 August 1989 – To complement analogous studies using conventional ligand‐membrane binding assays, the densities of γ‐aminobutyric acid and benzodiazepine receptors in the brain have been assessed using an autoradiographic technique in an animal model of hepatic encephalopathy. Hepatic encephalopathy due to fulminant hepatic failure was induced in rabbits by the intravenous injection of galactosamine.