Enhanced acetaminophen toxicity in rats with bilirubin glucuronyl transferase deficiency

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.

Increased bioavailability of enzymes of eicosanoid synthesis in hepatic and extrahepatic tissues after portacaval shunting

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.

Prolonged duck hepatitis B virus replication in duck hepatocytes cocultivated with rat epithelial cells: A useful system for antiviral testing

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.

Disseminated intravascular coagulation in cirrhosis

Justine Meehan Carr – 1 July 1989 – Hemorrhagic sequelae of liver disease were recognized and described over a century ago (1). Bleeding has been a common complication and a leading cause of death in patients with cirrhosis (2, 3). The coincidence of low clotting factor levels, hypofibrinogenemia and thrombo‐cytopenia has prompted many investigators to ask whether disseminated intravascular coagulation (DIC) plays a role in the pathogenesis of hemorrhage in these patients (4–16).

The portocardiorenal axis and refractory ascites: The underfilled cup runneth over

Charles L. Witte, Marlys H. Witte – 1 July 1989 – Plasma immunoreactive alpha‐human atrial natriuretic peptide (ANP) was measured in six cirrhotic patients with massive refractory ascites, under strict metabolic conditions, while they were receiving a 20‐meq sodium diet, both before and at two‐hour intervals for eight hours following peritoneovenous shunting (PVS). The mean preoperative level of ANP was 75±18pg/ml, which was found to be significantly higher than the normal range for this laboratory *8 to 24pg/ml) (p<0.05).

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