Abstract
The effect of nitrous oxide on neuronal cells during cerebral ischemia was evaluated by direct current (DC) potential, neuronal damage and dynamic change in extracellular glutamate concentration.
Under 1 % halothane anesthesia, forty-six male gerbils were randomly assigned to a group receiving 70% nitrous oxide (N2O group) and a group receiving 70% nitrogen (N2 group) . Forebrain ischemia was performed by occlusion of bilateral common carotid arteries for 3, 5 or 7 minutes. DC potential was recorded from the bilateral hippocampal CA1 regions. Histological evaluation was performed 5 days after the ischemia. Dynamic change in hippocampal extracellular glutamate in 5-minutes ischemia was also measured.
Onset time of ischemic depolarization was shorter in the N2O group (p<0.01) . In the case of 5-minute ischemia, the percentage of damaged neurons in the N2O group was higher (p<0.01) . However, the difference of dynamic changes in extracellular glutamate concentrations in both groups was not significant.
Nitrous oxide increased neuronal damage at 5-minutes ischemia in gerbils. However, there was no significant difference between the dynamic changes in extracellular glutamate concentration in both groups. The increase of neuronal damage by nitrous oxide was affected by reduction of onset time and a factor other than the amount of extracellular glutamate release.
