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Abstract
It has been hypothesized that the mechanism of hypoglycemic brain damage involves energy failure or excessive accumulation of excitatory neurotransmitters. To test these hypotheses, 1H nuclear magnetic resonance spectroscopy was employed to determine brain high-energy phosphates, carbohydrates, neurotransmitters, amino acids, and fatty acids during insulin-induced hypoglycemia in the neonatal dog. Reduction in brain glucose content was associated with an increase in blood/brain lactate ratio, as well as decreases in brain glutamate, aspartate, taurine, and inositol; however, no change was observed in GABA concentration or in brain energy state. In contrast to the adult experimental animal, brain tissue injury due to hypoglycemia is minimal in the neonatal animal. The mechanism of resistance to hypoglycemic brain injury may involve modulation of the rise of excitatory amino acids and decline in inhibitory neurotransmitters and high-energy phosphates.
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