ETOMIDATE DOES NOT ALTER RECOVERY AFTER ANOXIA OF EVOKED POPULATION SPIKES RECORDED FROM THE CA1 REGION OF RAT HIPPOCAMPAL SLICES

Background: Etomidate is an anesthetic agent that reduces the cerebral metabolic rate and causes minimal cardiovascular depression. Its abil ity to improve recovery after anoxia or ischemia is equivocal. An in v itro neuronal preparation was used to examine the action of etomidate on electrophysiologic and biochemical parameters during and after anox ia Methods: The Schaffer collateral pathway was stimulated, and a post synaptic evoked population spike was recorded from the CA1 pyramidal c ell layer of rat hippocampal slices. Etomidate or propylene glycol its solvent, was present 15 min before, during, and 10 min after anoxia A denosine triphosphate, sodium, and potassium concentrations were measu red at the end of anoxia in tissue treated with etomidate, propylene g lycol or with no added drugs. Results: Etomidate did not alter recover y after 6 min of anoxia The population spikes from untreated slices re covered to 32% of their preanoxic amplitude, and slices treated with 0 .5, 3, and 30 mu g/ml etomidate recovered to 24%, 35%, and 13%, respec tively. Slices treated with propylene glycol equivalent to that in 3 a nd 30 mu g/ml etomidate, recovered to 46% and 12%, respectively, and t his was not significantly different from untreated slices. Etomidate d id not attenuate the decrease in adenosine triphosphate concentrations during anoxia. The increase in sodium and the decrease in potassium d uring anoxia were significantly attenuated by 30 but not by 3 mu g/ml etomidate. Conclusions: A range of etomidate concentrations did not si gnificantly alter recovery of the evoked population spike after anoxia in rat hippocampal slices. A high concentration of etomidate did atte nuate the increase in sodium and the decrease in potassium during anox ia.