Secobarbital attenuates excitotoxicity but potentiates oxygen-glucose deprivation neuronal injury in cortical cell culture.
J Cereb Blood Flow Metab
; 13(5): 803-10, 1993 Sep.
Article
em En
| MEDLINE
| ID: mdl-8360287
ABSTRACT
We examined the effects of secobarbital and other sedative-hypnotic barbiturates on the neuronal death induced by exposure to excitatory amino acids or deprivation of oxygen or glucose in mouse cortical cell cultures. N-Methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4- isoxazolepropionate, and kainate toxicities were attenuated in a concentration-dependent fashion by high concentrations of secobarbital or thiopental. Antagonism of NMDA toxicity was not overcome by increasing NMDA concentration and not mimicked by gamma-aminobutyrate. Despite these antiexcitotoxic actions, secobarbital exacerbated the neuronal death induced by deprivation of either glucose alone or oxygen and glucose together; death induced by oxygen deprivation alone was little affected. Thiopental and methohexital also increased oxygen-glucose deprivation injury. A possible explanation for this injury potentiation was provided by the observation that secobarbital enhanced the cellular ATP depletion induced by combined oxygen-glucose deprivation. Deleterious effects on ATP production may counterbalance the protective effects of barbiturates under some conditions.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Secobarbital
/
Córtex Cerebral
/
Glucose
/
Hipóxia
/
Neurônios
/
Neurotoxinas
Limite:
Animals
Idioma:
En
Ano de publicação:
1993
Tipo de documento:
Article