Role of excitatory amino acid antagonists in the management of birth asphyxia.
Birth asphyxia is an important cause of permanent neuro-developmental disability. Asphyxia sets in course a progression of intracellular events which culminates in neuronal death, and this process may take up to 48 h to complete. Entry of calcium into the neurone appears to be the key to the cell death, and it is known that during asphyxia, excessive glutamate is released which stimulates the voltage-dependent N-methyl-D-aspartate (NMDA) receptor to open with an accumulation of excess intracellular calcium. MK-801 is a very effective NMDA receptor antagonist, and it has been shown that this drug prevents or significantly reduces the extent of cortical neurone infarction following experimental asphyxia in 7-day-old rat pups. Unfortunately, MK-801 is toxic to the pup, but newer NMDA receptor antagonists may offer the opportunity for neuroprotection in the human infant who has suffered severe birth asphyxia.
Levene
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Malcolm Levene Academic Unit of Paediatrics and Child Health, Department of Clinical Medicine, University of Leeds, UK.
D000596:Amino Acids / Q000037:antagonists & inhibitors*; D000818:Animals; D001238:Asphyxia Neonatorum / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D001921:Brain / Q000473:pathology; D016291:Dizocilpine Maleate / Q000009:adverse effects / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists; D005971:Glutamates / Q000378:metabolism; D018698:Glutamic Acid; D006801:Humans; D007231:Infant, Newborn; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors; D013569:Synapses / Q000378:metabolism
D000596:Amino Acids; D018691:Excitatory Amino Acid Antagonists; D005971:Glutamates; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid; D016291:Dizocilpine Maleate