Hepatic Encephalopathy, Hyperammonemia, and Ammonia Toxicity

1. Front Matter

   Pages i-viii

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2. Animal Models of Hepatic Encephalopathy and Hyperammonemia

   • Kevin D. Mullen, Sigurbjorn Birgisson, Reynaldo C. Gacad, Hari Conjeevaram

   Pages 1-10

3. Brain Metabolism in Encephalopathy Caused by Hyperammonemia

   • Richard A. Hawkins, Anke M. Mans

   Pages 11-21

4. In Vivo Brain Magnetic Resonance Imaging (MRI) and Magnetic Resonance Spectroscopy (MRS) in Hepatic Encephalopathy

   • R. A. F. M. Chamuleau, B. A. P. M. Vogels, D. K. Bosman, W. M. M. J. Bovée

   Pages 23-31

5. Role of the Cellular Hydration State for Cellular Function: Physiological and Pathophysiological Aspects

   • Dieter Häussinger, Wolfgang Gerok

   Pages 33-44

6. Astrocyte-Neuron Interactions in Hyperammonemia and Hepatic Encephalopathy

   • Jan Albrecht, Lidia Faff

   Pages 45-54

7. Spinal Seizures in Ammonia Intoxication

   • W. Raabe

   Pages 55-64

8. Molecular Mechanism of Acute Ammonia Toxicity and of its Prevention by L-Carnitine

   • Vicente Felipo, Elena Kosenko, María-Dolores Miñana, Goizane Marcaida, Santiago Grisolía

   Pages 65-77

9. Portal-Systemic Encephalopathy: a Disorder of Multiple Neurotransmitter Systems

   • Roger F. Butterworth

   Pages 79-88

10. The GABA Hypothesis — State of the Art

    • E. Anthony Jones, Cihan Yurdaydin, Anthony S. Basile

    Pages 89-101

11. Neuropharmacologic Modulation of Hepatic Encephalopathy: Experimental and Clinical Data

    • Peter Ferenci, Andreas Herneth, Andreas Püspök, Petra Steindl

    Pages 103-112

12. S-Adenosyl-L-Methionine Synthetase and Methionine Metabolism Deficiencies in Cirrhosis

    • José M. Mato, Luis Alvarez, Pablo Ortiz, Jesús Mingorance, Cristina Durán, María A. Pajares

    Pages 113-117

13. Diagnosis and Therapy of Hepatic Encephalopathy

    • Antoni Mas, Joan Manuel Salmerón, Joan Rodés

    Pages 119-123

14. Neomycin Reduces the Intestinal Production of Ammonia from Glutamine

    • Richard A. Hawkins, John Jessy, Anke M. Mans, Antonio Chedid, Mary R. DeJoseph

    Pages 125-134

15. N-Acetylglutamate Synthetase (NAGS) Deficiency

    • J. P. Colombo

    Pages 135-143

16. Ornithine Transcarbamylase Deficiency: A Model for Gene Therapy

    • Manal A. Morsy, C. Thomas Caskey

    Pages 145-154

17. Retroviral Gene Transfer for LDL Receptor Deficiency into Primary Hepatocytes

    • Jean-Christophe Pages, Marion Andreoletti, Myriam Bennoun, Dominique Franco, Pascale Briand, Anne Weber

    Pages 155-159

18. The “Carnitine System”: Recent Aspects

    • Noris Siliprandi, R. Venerando, V. Tassani

    Pages 161-164

19. Use of Hepatocyte Cultures for Liver Support Bioreactors

    • Jörg C. Gerlach

    Pages 165-171

20. Hepatitis C Viral Infection after Orthotopic Liver Transplantation

    • Joaquín Berenguer, Martín Prieto, José Mir, Juan Cordoba, Miguel Rayón

    Pages 173-179

This volume contains the papers presented at the International Symposium on "Cirrhosis, Hyperammonemia and Hepatic Encephalopathy", held in Valencia, Spain, January 24th-27th, 1994. Liver cirrhosis and other hepatic dysfunctions such as fulminant hepatic failure and congenital defects of urea cycle enzymes can lead to hepatic encephalopathy, coma and death. Hepatic encephalopathy is one of the main causes of death in western countries. The ability to detoxify ammonia by its incorporation into urea is diminished by impaired liver function, resulting in increased ammonia levels in blood and brain. Hyperammonemia is considered one of the main factors in the mediation of hepatic encephalopathy and the classical clinical treatments are directed towards reducing blood ammonia levels. However, the molecular bases of the pathogenesis of hepatic encephalopathy and the role of hyperammonemia in this process remain unclear and several hypotheses have been proposed. To clarify the mechanisms involved in hepatic encephalopathy and hyperammonemia suitable animal models are necessary. The animal models available and the ideal features of an animal model are presented in the initial part of the book.

• Pathogene
• brain
• death
• enzymes
• liver
• toxicity
• hepatology

• Instituto de Investigaciones Citologicas de la F. I. B., Valencia, Spain

  Vicente Felipo, Santiago Grisolia

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