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[Changes in brain metabolism in hepatic coma].

J M Funovics, D F Dedrick, J E Fischer

    Chirurgisches Forum Fur Experimentelle Und Klinische Forschung
    |April 1, 1977
    PubMed
    Summary
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    This study found that experimental hepatic coma in rats did not involve brain energy deficits. Instead, a decrease in excitatory amino acids like glutamate and aspartate was observed, challenging ammonia-based theories.

    Area of Science:

    • Neuroscience
    • Biochemistry
    • Pathophysiology

    Context:

    • Hepatic coma, a severe complication of liver disease, is characterized by altered brain function.
    • The pathogenesis of hepatic coma is not fully understood, with ammonia toxicity being a prominent hypothesis.
    • Previous research suggested ammonia accumulation disrupts brain energy metabolism.

    Purpose:

    • To investigate the cerebral energy metabolism and neurotransmitter levels during experimental hepatic coma in Sprague-Dawley rats.
    • To evaluate the validity of the ammonia toxicity hypothesis in the context of hepatic coma pathogenesis.
    • To identify key biochemical alterations in the brain during hepatic coma.

    Summary:

    • Controlled experiments in rats with hepatic coma for 6 hours revealed no shortage in main cerebral energy reserves; brain glycogen was elevated, while phosphocreatine, ATP, and glucose remained unchanged.

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  • No significant alterations were found in the intermediates of the glycolytic pathway and tricarboxylic acid cycle within brain tissue.
  • A significant decrease in brain glutamate and aspartate, key excitatory neurotransmitters, was observed, contradicting the established role of ammonia.

    • Impact:

    • These findings challenge the long-standing hypothesis attributing hepatic coma pathogenesis primarily to ammonia toxicity.
    • The study highlights the potential role of altered excitatory amino acid levels in hepatic encephalopathy.
    • Provides new insights into the neurochemical underpinnings of hepatic coma, suggesting alternative pathways for investigation.