Abstract: The aim was to observe the dynamic change of neuron-specific enolase activity a fter experim ental cerebral ischemia and the effect of hyperbaric oxygen (HBO) on it, and exp lore the mechanism of HBO therapy. Sprague Dawlay rats were randomly divided int o three groups: ischemia/reperfusion group (I/R), group treated by HBO (HBO) and sham operated group (Sham-O) as control. Global brain ischemia was induced usi ng a modified four-vessel occlusion model originally described by Pulsinelli an d Buchan. Blood was collected in EDTA respectively at reperfusion time of 6th h, 24th h, 48th h and 96th h after 20 min of ischemia, the NSE activity was measur ed by ELISA. The plasma NSE levels on 6th h and 96th h I/R groups were significant ly h igher than Sham-O group (P<0.05). These data suggest that plasma NSE increa sed after global ischemia/reperfusion. The increment of 6th h and 96th h presuma bly represented the acute neuronal necrosis and delayed neuronal death respectiv ely. Compared with 6th h I/R group, the NSE level on 6th h HBO group significantly de crea sed (P<0.05). There were no statistically significant differences between ot her HBO groups and corresponding I/R groups (P>0.05). These data indicate th at the recovery of NSE level in HBO group is earlier than I/R group. The optimal therapeutic window of HBO in this study is 6 h after reperfusion.

Key words: hyperbaric oxygen, cerebral ischemia, reperfusion, neuron-specific enolase, apoptosis