Proceedings of an international symposium held in Valencia, Spain, November 27--29, 1989

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Ammonia Metabolism.- 1. Cerebral Function in Hepatic Encephalopathy.- 2. Ammonia Metabolism in Normal and Portacaval Shunted Rats.- 3. Nitrogen Metabolism in Normal and Cirrhotic Liver.- Effects of Hyperammonemia on Brain.- 4. Hyperammonemia Induces Brain Tubulin.- 5. Astrocytes in Hepatic Encephalopathy.- 6. Effects of NH4+ on the Function of the CNS.- Neurotransmission in Hepatic Encephalopathy.- 7. Hepatic Encephalopathy, GABA-ergic Neurotransmission and Benzodiazepine Receptor Ligands.- 8. Neurotransmission in Hepatic Encephalopathy.- 9. Synaptic Plasma Membrane Composition and Fluidity in the Pathogenesis of Hepatic Encephalopathy.- Carnitine and Ammonium Toxicity.- 10. Metabolic Effects of Carnitine and Carnitine Analogs.- 11. Clinical Use of Carnitine. Past, Present and Future.- 12. New Roles of Carnitine Metabolism in Ammonia Cytotoxicity.- Clinical Aspects.- 13. Effect of L-Carnitine Upon Ammonia Tolerance Test in Cirrhotic Patients.- 14. Metabolism of Sedatives in Liver Disease.- 15. Branched Chain Amino Acids in the Treatment of Hepatic Encephalopathy.- 16. Treatment of Portal Systemic Encephalopathy: The Old and New Treatments.- 17. Benzodiazepine Antagonist in the Treatment of Human Hepatic Encephalopathy.- Contributors.

This volume contains the papers presented at the Inter national Symposium on "Cirrhosis, Hepatic Encephalopathy and Ammonium Toxicity", held in Valencia, Spain, November 27-29, 1989. Hepatic cirrhosis as well as other liver failures usual ly lead to hepatic encephalopathy which is an important cause of death in occidental countries. However the molecular bases of the pathogenesis of hepatic encephalopathy remain unclear and several hypotheses have been proposed. Hyperammonemia is considered one of the main factors responsible for the mediation of hepatic encephalopathy. Therefore, a part of the book is devoted to the effects of hyperammonemia on cerebral function, ammonia and amino acid metabolism, brain microtobules, astrocytes and synaptic trans mission and their possible role in the pathogenesis of hepatic encephalopathy. Carnitine has a remarkable protective effect against acute ammonium intoxication. Thus some results regarding this effect are also presented, as well as the clinical use of car nitine. The alterations of the metabolism of ammonia and of seda tives in liver diseases and their clinical implications are also discussed. The possible role of altered GABA-ergic neurotransmission on the pathogenesis of hepatic encephalopathy has received considerable attention recently. Results of these studies and those on benzodiazepine receptor ligands are presented as well as those on the hypothesis of the role of altered synaptic plasma membrane on the pathogenesis of hepatic encephalopathy.