Dennis L. Avner, … , Randall G. Lee, Malcolm M. Berenson
Citation Information: J Clin Invest. 1981;67(2):385-394. https://doi.org/10.1172/JCI110046.
Dennis L. Avner, … , Randall G. Lee, Malcolm M. Berenson
Published February 1, 1981
Citation Information: J Clin Invest. 1981;67(2):385-394. https://doi.org/10.1172/JCI110046.
Abstract
The pathogenesis of liver disease in protoporphyria has been presumed to result from the hepatic deposition of protoporphyrin. To examine the effects of protoporphyrin on hepatic bile flow and histopathology, studies were performed employing an isolated, in situ, rat liver perfusion system. Rat livers in the control group were perfused with 0-80 μmol sodium taurocholate/h. Rat livers in the experimental group were perfused with sodium taurocholate and (a) sufficient quantities of protoporphyrin to produce maximal canalicular secretion and (b) perfusate protoporphyrin concentrations of 0.01, 0.1, and 1 μM.
Authors
Dennis L. Avner, Randall G. Lee, Malcolm M. Berenson
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