Cortical excitatory amino acid release and cell function during hypotension in near-term born lambs.
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.


OBJECTIVE
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.


CONCLUSIONS
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.
Department of Pediatrics, University Medical Center Nijmegen, Nijmegen, The Netherlands.
Sandra
S
van Os
Wim
W
Ruitenbeek
Jeroen
J
Hopman
John
J
Klaessens
Margot
M
van de Bor
D000818:Animals; D000831:Animals, Newborn; D001224:Aspartic Acid / Q000378:metabolism; D001931:Brain Mapping; D002540:Cerebral Cortex / Q000378:metabolism* / Q000503:physiopathology*; D018846:Excitatory Amino Acids / Q000378:metabolism*; D045604:Extracellular Fluid / Q000378:metabolism; D005260:Female; D018698:Glutamic Acid / Q000378:metabolism; D019585:Intracranial Hypotension / Q000378:metabolism* / Q000503:physiopathology; D011247:Pregnancy; D012756:Sheep
D018846:Excitatory Amino Acids; D001224:Aspartic Acid; D018698:Glutamic Acid