BRAIN ION AND AMINO-ACID CONTENTS DURING EDEMA DEVELOPMENT IN HEPATIC-ENCEPHALOPATHY

Brain edema in hepatic encephalopathy has been associated with circula ting ammonia that is metabolized to glutamine. We measured alterations in blood chemistry and brain regional specific gravity and ion and am ino acid contents in models of simple hyperammonemia and liver failure induced by daily administrations of ammonium acetate (AAc) or thioace tamide (TAA), respectively. Serum and brain ammonia increased to simil ar levels (200 and 170% of control, respectively) in both experimental groups. Serum transaminase activities increased 10-fold in animals in jected with TAA but were unchanged in animals given AAc injections. In both experimental groups glutamine was elevated in cerebral white mat ter, cerebral gray matter, and basal ganglia, whereas brain tissue spe cific gravity decreased in all brain regions, indicating edema formati on. In the AAc group, we observed a decrease in glutamate and taurine contents concomitant with the development of brain edema. In these ani mals, cerebral gray matter specific gravity and taurine contents retur ned to control levels 24 h after the third AAc injection. TAA-injected animals demonstrated similar decreases in brain tissue specific gravi ty, whereas glutamine, glutamate, and taurine contents were all elevat ed. During hepatic encephalopathy, ammonia-induced changes in brain am ino acid content may contribute to brain edema development.