Biliary excretion of sulfobromophthalein compounds in normal and mutant corriedale sheep. Evidence for a disproportionate transport defect for conjugated sulfobromophthalein

James L. Barnhart, Ronald R. Gronwall, Burton Combes – 1 September 1981 – Biliary excretion of dye was evaluated in three normal and one mutant Corriedale sheep (characterized by depressed biliary transport of many organic anions) during infusion of unconjugated sulfobromophthalein (BSP) and its preformed glutathione conjugate (BSP‐GSH). Maximal dye excretion rates in bile in normal sheep were higher when BSP‐GSH rather than BSP was administered. In confirmation of earlier studies, dye excretion in bile was markedly depressed in the mutant animal.

Electron microscopic studies of Dane particles in hepatocytes with special reference to intracellular development of Dane particles and their relation with HBeAg in serum

Tomoteru Kamimura, Akira Yoshikawa, Fumihiro Ichida, Hiroshi Sasaki – 1 September 1981 – Electron microscopic observations in 30 cases of HBsAg positive liver disease and 12 asymptomatic carriers of HBsAg suggested the following mechanism of intracellular development of Dane particles: core particles migrated from the nucleus into the cytoplasm through the nuclear pores. Intracytoplasmic core particles protruded into the cisternae of endoplasmic reticulum by budding the outer coat of Dane particles being derived from the membrane of endoplasmic reticulum.

Hepatocyte and Kupffer cell functions during liver regeneration in streptozotocin‐diabetic rats

Robert P. Cornell, Brenda K. Hinck, Randall E. Halley – 1 September 1981 – The insulinoprivic influence of acute severe streptozotocin diabetes on liver regeneration in rats was evaluated by determining liver weights as well as hepatocyte and Kupffer cell functional capacities. Functional capacities were assessed by bromosulfophthalein uptake for hepatocytes and carbon phagocytosis for Kupffer cells.

The hepatocellular uptake and biliary excretion of endotoxin in the rat

Shyamal K. Maitra, Daniel Rachmilewitz, David Eberle, Neil Kaplowitz – 1 September 1981 – Endotoxin is known to cause a dose‐dependent impairment of hepatic bile secretion, organic anion excretion, and activity of Na+, K+‐activated ATPase. Since it is possible that this impaired excretory function is a result of direct interaction of endotoxin with hepatocytes, we examined: (a) the excretion of endotoxin into bile, and (b) its association with an hepatocyte‐enriched, Kupffer cell‐depleted population of liver cells.

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