An anesthetized model of lethal canine galactosamine fulminant hepatic failure

Timothy D. Sielaff, Michael Y. Hu, Mark D. Rollins, Joseph R. Bloomer, Bruce Amiot, Wei Shou Hu, Frank B. Cerra

Research output: Contribution to journalArticlepeer-review

52 Scopus citations


A reproducible large animal model of fulminant hepatic failure was developed in the anesthetized dog by the administration of the amino sugar D-galactosamine. Galactosamine in 5% dextrose in water (D5W), was given as an intravenous bolus to 10 young male dogs weighing 27 to 30 kg. Three dogs that received an equal volume of D5W alone served as controls. Galactosamine at 0.5 g/ kg (n = 5) produced significant biochemical evidence of liver injury with 100% survival at 48 hours. Galactosamine 1.0 g/kg (n = 5) yielded in 100% 48-hour mortality resulting from fulminant liver failure characterized by a progressive increase in liver enzymes, total bilirubin, ammonia, and lactate and associated coagulopathy, hypoglycemia, coma, and increased intracranial pressure. Necropsy showed liver pallor, ascites, and brain swelling. Liver histology showed significant hepatocellular necrosis. This clinically relevant large animal model will enable the quantitative evaluation of new technologies, such as the bioartificial liver, for the support of hepatic failure in humans.

Original languageEnglish (US)
Pages (from-to)796-804
Number of pages9
Issue number3
StatePublished - Mar 1995

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