Excitatory amino acid release and electrocortical brain activity after hypoxemia in near-term lambs

Brain & Development
Sandra van OsMargot van de Bor

Abstract

Energy failure due to insufficient cerebral O(2)-supply leads to excess accumulation of calcium ions in presynaptic neurons, followed by excess release of excitatory amino acids (EAAs), which are potent neurotoxins, into the synaptic cleft. The aim of the present study was to determine whether extracellular EAAs release after prolonged hypoxemia affects electrocortical brain activity (ECBA), as a measure of brain cell function, in near-term born lambs. Ten near-term lambs (term: 147 days) were delivered at 131 days of gestation. After a stabilization period, prolonged hypoxemia (FiO(2): 0.10; duration 2.5h) was induced. Mean values of physiologic variables, including ECBA, were calculated over the last 3 min of normoxemia as well as of hypoxemia. Cerebral arterial and venous blood gases were determined at the end of the normoxemic and hypoxemic periods. Cerebrospinal fluid (CSF) was obtained at the end of the hypoxemic period. CSF from six normoxemic sibs was used for comparison. HPLC was used to measure EAAs in the CSF. During hypoxemia, aspartate and glutamate concentration increased significantly (4.8 and 6.0 times, respectively), while asparagine and glutamine did not. ECBA decreased to 30% of the normoxemic value. Glutamat...Continue Reading

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Citations

Nov 26, 2009·Naunyn-Schmiedeberg's Archives of Pharmacology·Chen-Jing WangYuan-Jian Li
Jan 21, 2012·European Journal of Paediatric Neurology : EJPN : Official Journal of the European Paediatric Neurology Society·Xiao-Yu WangXiao-Ming Wang

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