Excitatory amino acids and magnesium sulfate in neonatal asphyxia

Objective. The excitatory amino acids (EAA); glutamate and aspartate are released into the cerebrospinal fluids (CSF) of asphyxiated newborns. The objectives of this study were: (a) to examine the relation of the concentration of EAA in the CSF with the degree of brain injury, (b) To determine the t...

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Bibliographic Details
Published in:Brain & development (Tokyo. 1979) 2006-07, Vol.28 (6), p.375-379
Main Authors: Khashaba, Mohamed T., Shouman, Basma O., Shaltout, Ali A., Al-Marsafawy, Hala M., Abdel-Aziz, Mohamed M., Patel, Kantilal, Aly, Hany
Format: Article
Language:English
Subjects:
Anticonvulsants - administration & dosage
Aspartate
Aspartic Acid - cerebrospinal fluid
Asphyxia Neonatorum - cerebrospinal fluid
Asphyxia Neonatorum - drug therapy
Female
Glutamate
Glutamic Acid - cerebrospinal fluid
Humans
Hypoxia, Brain - cerebrospinal fluid
Hypoxia, Brain - drug therapy
Hypoxic ischemic encephalopathy
Infant, Newborn
Magnesium Sulfate - administration & dosage
Male
MgSO 4
Prospective Studies
Randomized trial
Severity of Illness Index
Treatment Failure
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Summary:Objective. The excitatory amino acids (EAA); glutamate and aspartate are released into the cerebrospinal fluids (CSF) of asphyxiated newborns. The objectives of this study were: (a) to examine the relation of the concentration of EAA in the CSF with the degree of brain injury, (b) To determine the time of the release of these EAA into the CSF, and (c) to detect the effect of magnesium sulfate (MgSO 4) on their levels. Designs and methods. A randomized controlled trial was conducted on 47 full term asphyxiated newborns. Twenty three infants received an intravenous 10% solution of MgSO 4 at a dose of 250 mg/kg within the first 24 h of life while the other 24 newborns received isotonic saline (0.9%) of an equal volume. Levels of glutamate and aspartate were measured before and 72 h after giving the trial solution. Results. In the study population ( n=47) both glutamate and aspartate were significantly elevated in infants with higher grades of HIE compared to those with lower grades ( P=0.013 and 0.031, respectively). Compared to baseline level, glutamate decreased significantly over time in placebo group (−8.28±14.26, P=0.025) and in MgSO 4 group (−14.39±18.72, P=0.005). Glutamate concentration did not differ between groups when measured at baseline (29.26±16.31 vs. 31.27±22.62, P=0.82) and at 72 h (19.28±15.63 vs. 19.6±16.54, P=0.87). The change in aspartate concentration over time was not significant in placebo group (−0.45±1.96, P=0.34) or in MgSO 4 group (−0.7±3.19, P=0.37). Aspartate did not differ between groups when measured at baseline (3.52±2.4 vs. 3.92±2.59, P=0.49) or at 72 h (2.79±1.24 vs. 3.05±2.48, P=0.92). Conclusions. The EAA; glutamate and aspartate are released in the CSF of asphyxiated newborns immediately after birth and declined by 72 h. Their initial concentrations correlated with the severity of HIE. Postnatal administration of MgSO 4 did not alter the levels of these 2 EAA.
ISSN:0387-7604
1872-7131
DOI:10.1016/j.braindev.2005.11.010