This volume contains the papers presented at the International Symposium on Cirrhosis
Hyperammonemia and Hepatic Encephalopathy held in Valencia Spain De cember 2nd_4th 1996.
Liver cirrhosis is one of the main causes of death in occidental countries. There are other
hepatic dysfunctions such as fulminant hepatic failure Reye's syndrome or congenital
deficiencies of urea cycle enzymes which can also lead to hepatic encephalopathy coma and
death. However the molecular bases ofthe pathogenesis of hepatic encephalopathy remain
unclear. One ofthe consequences of hepatic failure is the reduced ability to detoxify ammonia
by incorporating it into urea. This leads to increased blood ammonia levels. Hyperam monemia is
considered one of the main factors responsible for the mediation of hepatic encephalopathy and
classical clinical treatments are directed towards reducing blood ammo nia levels. Altered
neurotransmission is an essential step in the pathogenesis of hepatic encephalopathy. The first
part of the book is devoted to the discussion of the recent advances in the understanding of
the alterations of different neurotransmitter systems in hepatic encephalopathy. The
alterations of tryptophan metabolism and neurotransmission in hepatic encephalopathy and the
implications for the clinical use of neuropsychoactive drugs are reviewed. The alterations in
glutamate transport and neurotransmission in hepatic encephal opathy due to acute liver failure
are also reviewed. The role of NMDA receptors in the molecular mechanism of acute ammonia
toxicity is discussed as well as its modulation by metabotropic glutamate receptors and
muscarinic receptors.
