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Canadian Journal of Gastroenterology
Volume 5, Issue 6, Pages 219-223
Experimental Gastroenterology

Early Hepatic Dysfunction in a Large Animal Model of Nonhypotensive Sepsis

Stephen Sullivan, Michael Troster, and Adam Linton

Department of Medicine and Pathology, Victoria Hospital, London, Ontario, Canada

Received 31 May 1991; Accepted 8 November 1991

Copyright © 1991 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Sepsis was induced in 12 sheep by cecal devascularization and perforation. Intravenous crystalloid was administered to maintain th e pulmonary capillary wedge pressure at preseptic levels. By 24 h there was a significant drop in albumin and alkaline phosphatase with increases in aspartate aminotransferase (AST), lactate dehydrogenase and bilirubin. By 48 h the alkaline phosphatase had returned to presepsis levels, the bilirubin continued to rise, the AST and lactate dehydrogenase had plateaued while the alhumin remained low. These biochemical alterations were confirmed by examining data from 25 sheer used in similar sepsis experiments. These data revealed that marked elevations in AST were associated with a higher central venous pressure and worse renal impairment, but there was no relationship with any other hemodynamic parameter, PO2, pH or serum lactate. Histologically these biochemical alterations were associated with extensive microvesicular fatty change at 24 h and centrilobular necrosis at 48 h. Electron microscopy revealed mitochondrial degeneration, hyperplasia of the smooth endoplasmic reticulum and intracellular cholestasis.