A Prospective Morphologic Evaluation of Hepatic Toxicity of Chenodeoxycholic Acid in Patients with Cholelithiasis: The National Cooperative Gallstone Study

Rosemarie L. Fisher, Deborah W. Anderson, James L. Boyer, Kamal Ishak, Gerald Klatskin, John M. Lachin, M. James Phillips, The Steering Committee, The National Cooperative Gallstone Study Group – 1 March 1982 – A sample of 126 patients with cholelithiasis was treated with chenodeoxycholic acid (CDCA) (375 or 750 mg g.d.) for 2 years. Hepatotoxicity was assessed by sequential light (LM) and electron microscopic (EM) analysis of liver biopsies obtained before and after 9 and 24 months of therapy.

Triton WR‐1339, A Lysosomotropic Compound, Is Excreted into Bile and Alters the Biliary Excretion of Lysosomal Enzymes and Lipids

Nicholas F. Larusso, Louis J. Kost, Janet A. Carter, Steven S. Barham – 1 March 1982 – In these experiments, we tested two hypotheses: first, that Triton WR‐1339, a nonionic detergent which is sequestered in hepatocyte lysosomes, undergoes biliary excretion; and second, that Triton WR‐1339, which also alters serum lipid levels and modifies hepatic catabolism of lipoproteins, affects the biliary output of proteins and lipids.

Effects of Ticrynafen on Hepatic Excretory Function in the Isolated Perfused Rat Liver

Hyman J. Zimmerman, Charles O. Abernathy, Lorinc Lukacs, Mildred Ezekiel – 1 March 1982 – Ticrynafen, a uricosuric diuretic agent which causes hepatocellular injury in man as an apparent idiosyncratic reaction, was found to impair the function of the isolated perfused rat liver. At concentrations in the perfusate equivalent to those produced in the blood of man by therapeutic doses, the drug led to a striking reduction in bile flow and sulfobromophthalein excretion and release of aspartate aminotransferase into the perfusate.

The Relationship Between Prostacyclin Activity and Pressure in the Portal Vein

George Hamilton, Rose Chow Fung Phing, Ronald A. Hutton, Paresh Dandona, Kenneth E. F. Hobbs – 1 March 1982 – The effect of portal hypertension (induced by partial ligation) on the ability of the portal vein wall to produce prostacyclin (PGI2) was studied in rats over a period of 6 weeks. PGI2‐like activity measured by bioassay was shown to be significantly increased in portal vein segments during established hypertension when compared to control groups. As a collateral circulation developed with consequent fall in portal venous pressure, PGI2‐like activity decreased.

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