Abstract
A subacute experimental model of hepatic encephalopathy was created in the rat by constructing a portacaval shunt with subsequent gavage feeding of a cationic ammonium exchange resin. The clinical course was characterized by fluctuating levels of consciousness, bizarre behavior, and motor symptoms leading to coma and death. Histopathologically, proliferation of Alzeimer type II astrocytes in the cerebral cortex was demonstrated. Serum ammonia levels were greatly elevated. This model should be useful in providing a better understanding of the pathogenesis of hepatic coma, and particularly the role of the astrocyte in this process.
