Physiologic and morphologic natural history of a model of intrahepatic cholestasis (manganese-bilirubin overload).
Study of the morphologic and physiologic features of the biliary excretory apparatus at 24 and 48 hours after the induction of intrahepatic cholestasis by manganese-bilirubin overload shows that at the same time that physiologic cholestasis is rapidly waning, morphologic features of cholestasis are, in fact, increasing. These observations therefore provide the first direct proof of the proposal that such features are not, in fact, causes of cholestasis, at least at its outset. Although morphologic and physiologic features do not parallel one another in time, they do seem to parallel one another in severity. Morphologic features in manganese-bilirubin cholestasis closely resemble those in human cholestasis, and so reaffirm the validity and potential value of manganese-bilirubin overload as a model for the study of cholestasis. However, a review of information available about these features, reveals little conclusive evidence as to their pathogenesis and biochemical connotations.
D000818:Animals; D001646:Bile; D001653:Bile Ducts, Intrahepatic / Q000473:pathology* / Q000503:physiopathology; D001663:Bilirubin; D002779:Cholestasis / Q000139:chemically induced / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology*; D004195:Disease Models, Animal; D008297:Male; D008345:Manganese; D008854:Microscopy, Electron; D051381:Rats; D012212:Rheology
D008345:Manganese; D001663:Bilirubin