Cimetidine inhibits the formation of the reactive, toxic metabolite of isoniazid in rats but not in man

Bernhard H. Lauterburg, Elizabeth L. Todd, Charles V. Smith, Jerry R. Mitchell – 1 July 1985 – The hepatotoxicity of isoniazid in rats results from the metabolic activation of acetylhydrazine, a metabolite of isoniazid, by the cytochrome P450 monooxygenase system. Inhibition of the drugmetabolizing enzyme system with a compound suitable for clinical use such as cimetidine might therefore prevent liver injury in experimental animals and in patients on isoniazid without interfering with the antituberculous activity of the drug.

Recovery of liver function in partially hepatectomized rats evaluated by aminopyrine demethylation capacity

I. Sendama, B. de Hemptinne, L. Lambotte – 1 July 1985 – Aminopyrine demethylation was investigated in rats after a 70% hepatectomy to assess possible parallelism between the recovery of mass and function. Tests were performed by analyzing 14CO2 exhalation from 0.1 μCi per 100 gm of body weight of [dimethylamine‐14C]aminopyrine given intraperitoneally with incremental doses of unlabeled drug.

Localization of increased hepatic vascular resistance in liver cirrhosis

Yuro Shibayama, Katsuji Nakata – 1 July 1985 – To determine the localization of increased vascular resistance in cirrhotic liver, blood pressures were measured by a direct cannulation method at several key points in the hepatic vascular pathway in normal and cirrhotic rats. Cirrhosis was produced by feeding a choline‐deficient diet. Blood pressures in normal rats were 110 mm H2O in the portal vein, 68 mm H2O in the terminal portal venule, 28 mm H2O in the terminal hepatic venule and 20 mm H2O in the inferior vena cava.

Portal venous bile acids in cholesterol gallstone disease: Effect of treatment with chenodeoxycholic and cholic acids

Kurt Einarsson, Jon Ahlberg, Bo Angelin, Ingemar Björkhem, Staffan Ewerth – 1 July 1985 – We determined the serum concentrations of cholic, chenodeoxycholic and deoxycholic acids in portal and peripheral venous blood in 9 gallstone‐free patients and 39 patients with cholesterol gallstones during standardized cholecystectomy. An accurate and specific gas chromatographic‐mass spectrometric technique was used.

Choline fails to prevent liver fibrosis in ethanol‐fed baboons but causes toxicity

Charles S. Lieber, Maria A. Leo, Ki M. Mak, Leonore M. Decarli, Shinkichi Sato – 1 July 1985 – To determine how choline supplementation affects the liver and whether it can protect against ethanol‐induced liver injury, baboons were fed either normal or choline‐supplemented diets, each with or without ethanol. Eighteen baboons were pair‐fed for 3 to 4 years liquid diets with 50% of total energy as ethanol or isocaloric carbohydrate; ten animals were given our regular diets, whereas in eight the choline content was increased 5‐fold.

Maternal transmission of duck hepatitis B virus in pedigree pekin ducks

Kwesi N. Tsiquaye, Thomas F. McCaul, Arie J. Zuckerman – 1 July 1985 – A 14‐month old female Pekin duck experimentally infected as an embryo with duck hepatitis B virus via the amniotic route has been a chronic carrier of duck hepatitis B virus with very high (P/N) values of DNA polymerase activity since hatching. All the progeny were, on evaluation for congenital infection, found to be duck hepatitis B virus positive by endogenous DNA polymerase reaction and electron microscopy. These offspring remained persistently viremic throughout the study.

A prospective, randomized controlled trial of chronic esophageal variceal sclerotherapy

Jacob Korula, Luis A. Balart, George Radvan, Bruce E. Zweiban, Alan W. Larson, Henry W. Kao, Suyenori Yamada – 1 July 1985 – The results of a prospective, randomized controlled trial of chronic esophageal variceal sclero‐therapy conducted over a 38‐month period are presented. One‐hundred twenty patients were randomized following variceal bleeding, 63 to esophageal variceal sclerotherapy and 57 to control. Mean follow‐up was similar in both groups (esophageal variceal sclerotherapy, 12.5 ± 8.8 months; control, 14.9 ± 6.6 months).

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