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Cortical Excitatory Amino Acid Release and Cell Function during Hypotension in Near-Term Born Lambs

Authors
  • van Os, Sandra
  • Ruitenbeek, Wim
  • Hopman, Jeroen
  • Klaessens, John
  • van de Bor, Margot
Type
Published Article
Journal
Neonatology
Publisher
S. Karger AG
Publication Date
Aug 10, 2006
Volume
90
Issue
2
Pages
128–134
Identifiers
DOI: 10.1159/000092450
PMID: 16582537
Source
Karger
Keywords
License
Green
External links

Abstract

Background: Energy failure due to insufficient cerebral O2-supply leads to excess accumulation of calcium ions in presynaptic neurons, followed by excess release of excitatory amino acids, which are potent neurotoxins, into the synaptic cleft. Aim:To investigate whether electrocortical brain activity (ECBA) can provide an adequate measure for excitatory amino acid release due to hemorrhagic hypotension. Methods: Ten near-term lambs were delivered at 127 days of gestation (term: 147 days). After a stabilization period, hypotension was induced by stepwise withdrawal of blood. Cerebral microdialysis was used to measure the concentrations of glutamate and aspartate. Results:During hypotension, mean arterial blood pressure, cerebral O2-supply and ECBA decreased and the extracellular concentration of glutamate increased significantly. ECBA was significantly related to glutamate (R2: 0.67, p < 0.001) and aspartate (R2: 0.57, p < 0.001) concentrations. Conclusion:The extracellular release of glutamate and aspartate in the cerebral cortex increases after hemorrhagic hypotension in near-term born lambs. The extracellular overflow of glutamate and aspartate were significantly inversely related to ECBA.

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