Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add filters








Language
Year range
1.
Korean Journal of Anesthesiology ; : 794-801, 2001.
Article in Korean | WPRIM | ID: wpr-32416

ABSTRACT

BACKGROUND: The present investigation was undertaken to evaluate the neuroprotective effect of etomidate against kainic acid (KA) induced neurotoxicity in rats by using the immunoreactivity of heat shock protein-70 (HSP-70) and the acid-fuchsin stain. METHODS: Administration of etomidate (20 mg/kg, I.P.) was performed in sequence; first being just one hour after a KA (10 mg/kg, I.P.) injection, then three more times at one hour intervals. Neuronal damages in the hippocampus were evaluated by using the acid-fuchsin stain to detect cell death and HSP-70 induction as an index of cell injury at 24 h after the administration of KA. RESULTS: HSP-70 induction and acid fuchsin positive neurons were increased in the CA1 and CA3 regions of the hippocampus after a KA injection but significantly decreased by an injection of etomidate (P < 0.01). CONCLUSIONS: These results suggest that the etomidate has a potential effect on the protection of neurons against KA-induced neurotoxicity.


Subject(s)
Animals , Rats , Cell Death , Etomidate , Hippocampus , Hot Temperature , Kainic Acid , Neurons , Neuroprotective Agents , Rosaniline Dyes , Shock
2.
Korean Journal of Anesthesiology ; : 698-705, 1996.
Article in Korean | WPRIM | ID: wpr-72623

ABSTRACT

BACKGROUNDS: The importance of toxic extracellular levels of excitatory amino acids, as well as of high extracellular levels of inhibitory amino acids, is considered to be related with the pathophysiology of neuronal cell loss during cerebral ischemia. METHODS: The extracellular concentration of glutamate, glycine, and taurine in the hippocampus were determined during and after transient global ischemia in the New Zealand white rabbit. Because the cerebroprotective effects of profound hypothermia are well known and clinically widely used,we used the hypothermia group as an experimental group compared with normothermic control group in the experimental protocol. To derive a quantitative descriptor reflecting the magnitude of amino acid neurotransmitter changes with ischemia, we defined the 'taurine index' as: [glutamate]x[glycine]/[taurine]. RESULTS: Ischemia led to large increases in both excitatory (glutamate and glycine) and inhibitory amino acids(taurine) in the normothermic group. Taurine index was increased during ischemia and after reperfusion and had a close relationship with the severity of ischemia-induced neuronal damage. CONCLUSIONS: The taurine index appears to be a reliable biochemical marker to determine the severity of ischemic injury.


Subject(s)
Amino Acids , Biomarkers , Brain Ischemia , Excitatory Amino Acids , Glutamic Acid , Glycine , Hippocampus , Hypothermia , Ischemia , Neurons , Neurotransmitter Agents , New Zealand , Reperfusion , Subject Headings , Taurine
SELECTION OF CITATIONS
SEARCH DETAIL