Dr. R. A. Kauppinen is on a leave of absence from the Department of Clinical Neurophysiology, University Central Hospital of Kuopio, Kuopio, Finland.
Observation of Cerebral Metabolites in an Animal Model of Acute Liver Failure In Vivo: A 1H and 31P Nuclear Magnetic Resonance Study
Version of Record online: 5 OCT 2006
Journal of Neurochemistry
Volume 53, Issue 1, pages 102–110, July 1989
How to Cite
Bates, T. E., Williams, S. R., Kauppinen, R. A. and Gadian, D. G. (1989), Observation of Cerebral Metabolites in an Animal Model of Acute Liver Failure In Vivo: A 1H and 31P Nuclear Magnetic Resonance Study. Journal of Neurochemistry, 53: 102–110. doi: 10.1111/j.1471-4159.1989.tb07300.x
- Issue online: 5 OCT 2006
- Version of Record online: 5 OCT 2006
- Received September 13, 1988; revised manuscript received November 20, 1988; accepted accepted December 7, 1988
- Acute liver failure;
- Brain energy metabolism;
- Brain amino acids;
- Nuclear magnetic resonance
Abstract: Acute liver failure was induced in rats by a single intragastric dose of carbon tetrachloride. This causes hepatic centrilobular necrosis, as indicated by histological examinations, and produces a large increase in the activity of serum alanine aminotransferase. The plasma NH4+ level (mean ±SEM) was 123 ± 10 μM the control group and 564 ± 41 μM in animals with acute liver failure (each n = 5). 31P nuclear magnetic resonance (NMR) was used to monitor brain cortical high-energy phosphate compounds, Pi, and intracellular pH. 1H NMR spectroscopy was utilised to detect additional metabolites, including glutamate, glutamine, and lactate. The results show that the forebrain is capable of maintaining normal phosphorus energy metabolite ratios and intracellular pH despite the metabolic challenge by an elevated blood NH4+level. There was a significant increase in the brain glutamine level and a concomitant decrease in the glutamate level during hyperammonaemia. The brain lactate level increased twofold in rats with acute liver failure. The results indicate that 1H NMR can be used to detect cerebral metabolic changes in this model of hyperammonaemia, and our observations are discussed in relation to compartmentation of NH4+ metabolism.