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Rosemary Hickman, MD
Cape Town, South Africa

Arch Surg. 2000;135:1189.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Acute liver failure caused by fulminant hepatitis has at least 2 components—severe impairment or absence of liver function, and the effects of tissue destruction. The former effect can be simulated by rendering animals anhepatic. With adequate restoration of vascular connections, such animals will awake from anesthesia and appear normal for up to 60 hours. Even terminally, such animals seldom show features of hepatic encephalopathy, but rather of respiratory failure. This model is reasonably easy to reproduce; not so the attempts to use toxins or ischemia to simulate a human disease that probably occurs with recurrent waves of destruction compounding damage.

For more than 40 years, attempts have been made to simulate human acute liver failure to test forms of treatment, including extracorporeal liver perfusion in the 1970s and liver transplantation or the bioartificial liver in the 1980s and 1990s. The report by Fourneau et al adds to . . . [Full Text of this Article]

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An Improved Model of Acute Liver Failure Based on Transient Ischemia of the Liver
Inge Fourneau, Jacques Pirenne, Tania Roskams, and Sing-Hiem Yap
Arch Surg. 2000;135(10):1183-1189.
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