Ito M, Matsumoto H, Kikuchi S, Yachi A
No To Shinkei. 1986 Jan;38(1):63-8.
In order to elucidate the role of amino acid changes in hepatic encephalopathy, free amino acids in serum and cerebral cortex were measured in the experimental hepatic failure models. The acute and chronic models were produced in adult male Wistar rats by carbontetrachloride (CCl4) administration. Acute model was produced by a single intraperitoneal injection of CCl4 (0.35 ml/100 g, B.W.) after the daily pretreatment of phenobarbital (6 mg/100 g, B.W.) for 4 days, while chronic model was established by successive injections CCl4 (0.20 ml/100 g, B.W., twice/week) for 13 weeks. They were confirmed to develop chemical changes compatible with hepatic failure, showing markedly elevated serum levels of NH3, GOT and ALP. Animals were killed by decapitation during fasting and the brains were removed immediately. The parietal cortexes were homogenized in 75% ethanol and deproteinized with water saturated chloroform. The supernatants were subjected to amino acid analyzer. In serum, almost all amino acid concentrations were elevated in acute hepatic failure, reflecting massive release of amino acids from severely damaged liver cells. Chronic hepatic failure rats, however, showed moderately elevated levels of valine and leucine and markedly high levels of phenylalanine and tyrosine, which eventually led to a reduction of the ratio of branched chain amino acids to aromatic amino acids. Regarding urea cycle related amino acids, there were decreases of aspartate and arginine and an increase of ornithine, while citrulline was not affected. In cerebral cortex, no different pattern was observed in acute heptic failure with the exception of increases in threonine, glycine and leucine.(ABSTRACT TRUNCATED AT 250 WORDS)
