Effect of halothane in cortical cell cultures exposed to N-methyl-D-aspartate.

摘要: In vivo studies have shown potent protection by volatile anesthetic agents against cerebral ischemic insults. Volatile also been to antagonize glutamatergic neurotransmission at the N-methyl-D-aspartate (NMDA) receptor. This study examined potential for halothane reduce neuronal excitotoxic lesions caused NMDA. Fetal rat cortical cell cultures were allowed mature 13–16 d. Culture wells (n = 13–16) treated with 0 mM – 3.96 in presence/absence of 30 μM Additional exposed NMDA 10 MK-801 or μ ACEA 1021. Cellular lethality was assessed measurement lactate dehydrogenase (LDH) 24 hrs later. A maximal effect observed 0.70 (2.1 vol%) wherein a 36% reduction NMDA-stimulated LDH release occurred relative untreated controls. Both and 1021 complete inhibition release. These data confirm that has modulatory effects receptor but potency this drug is less than specific antagonists either glutamate glycine. findings suggest can be partially explained anti-excitotoxic properties although other mechanisms action are probably important.