Effects of anesthetic agents on bile pigment excretion in the rat

Authors

  • Glenn R. Gourley M. D.,

    Corresponding author
    1. Departments of Pediatrics and Physiological Chemistry, University of Wisconsin, School of Medicine, Madison, Wisconsin 53792
    • University of Wisconsin Clinical Science Center (H4/474), 600 Highland Avenue, Madison, Wisconsin 53792
    Search for more papers by this author
  • William Mogilevsky,

    1. Departments of Pediatrics and Physiological Chemistry, University of Wisconsin, School of Medicine, Madison, Wisconsin 53792
    Search for more papers by this author
  • Richard A. Arend,

    1. Departments of Pediatrics and Physiological Chemistry, University of Wisconsin, School of Medicine, Madison, Wisconsin 53792
    Search for more papers by this author
  • Frank L. Siegel,

    1. Departments of Pediatrics and Physiological Chemistry, University of Wisconsin, School of Medicine, Madison, Wisconsin 53792
    Search for more papers by this author
  • Gerard B. Odell

    1. Departments of Pediatrics and Physiological Chemistry, University of Wisconsin, School of Medicine, Madison, Wisconsin 53792
    Search for more papers by this author

Abstract

Anesthesia-induced alterations in bilirubin conjugation were studied. Rats were fitted with bile duct and jugular vein catheters while anesthetized with diethyl ether, ketamine or pentobarbital. As anesthesia abated, bile was collected for the next 5 hr and analyzed for flow rate, total bilirubin excretion and bilirubin glucuronide composition. The high-performance liquid chromatography method used allowed direct analysis of bile without derivatization or extraction. Ether anesthesia was associated with a reversible suppression of diglucuronide formation and total bilirubin excretion, with reciprocal monoglucuronide changes. Bile flow and pigment excretion were variable with ketamine. Pentobarbital provided the most uniform excretion data, although the ratio of C-8:C-12 monoglucuronide varied with all drugs. These data are consistent with recently reported drug-induced alterations in hepatic uridine diphosphoglucuronic acid concentration and support the hypothesis that alterations in this substrate concentration are capable of influencing rates of hepatic glucuronide formation.

Ancillary