THE EFFECT OF ISOFLURANE ON BIOCHEMICAL-CHANGES DURING AND ELECTROPHYSIOLOGICAL RECOVERY AFTER ANOXIA IN RAT HIPPOCAMPAL SLICES

It is unclear whether isoflurane protects against neuronal damage. Thi s study examines the extent and mechanism by which isoflurane might af fect anoxic neuronal damage. The size of the evoked postsynaptic popul ation spike recorded from the CA I pyramidal cell layer of the rat hip pocampal slice 60 min after anoxia was compared with its preanoxic, pr eisoflurane level. Intracellular adenosine triphosphate (ATP), sodium, and potassium levels were measured in the dentate and CA 1 regions at the end of the anoxic period in similarly treated slices. Isoflurane increased the latency and reduced the amplitude of the evoked response before anoxia. Isoflurane (2%) did not significantly improve recovery of the evoked response after 5 min of anoxia (untreated slices = 6 +/ - 2 % (mean +/- SEM), isoflurane = 17 +/- 7 %); 1.5% isoflurane also d id not significantly improve recovery after 4 min of anoxia (untreated = 30 +/- 8 % vs. 1.5% isoflurane = 47 +/- 12 %). Isoflurane did not s ignificantly attenuate the decrease in ATP levels in either the dentat e or CA 1 regions of the hippocampal slice during 4 or 7 min of anoxia : however, there tvas a significant improvement in ATP levels after 10 min of anoxia in both regions of isoflurane-treated preparations (1.0 +/- 0.1 vs. 1.4 +/- 0.1, CA 1; 1.3 +/- 0.1 vs. 2.0 +/- 0.2 mM/mg dry weight, dentate). Sodium concentrations increased and potassium concen trations decreased during anoxia. Isoflurane did not significantly att enuate the changes in these ions during anoxia. in conclusion, isoflur ane does not significantly improve recovery of CA 1 pyramidal cells du ring anoxia nor does it attenuate the anoxic changes in ATP, sodium;an d potassium after 4 or 7 min of anoxia. With a more prolonged period o f anoxia (10 min) isoflurane reduces the decrease in ATP levels.