Objective To evaluate the neurotransmitter mechanism and protective efficiency of three methods of isoflurane intervention
on global cerebral ischemia, and to seek an effective method to improve cerebral ischemia damage. Methods Adult male Sprague-Dawley rats were randomly divided into sham operation group, control groups,
preconditioning groups, protective groups and resuscitation groups. The rats of the last four groups were further divided into 10, 15 and 20min ischemia subgroups. The model of global cerebral ischemia and reperfusion was reproduced in waking rats 2 days before ischemia. The
microdialysis samples were collected and BIS was recorded after reperfusion. The recovery of right reflection was observed after ischemia and the motor function was observed. All viable and apoptotic neurons were counted and the percentage of apoptotic neurons was calculated. The results showed that glutamate concentration in the hippocampus of protective groups was significantly lower compared with preconditioning group and resuscitation group. Results With ischemia fasting 10 and 15min (P<0.01), and glutamate concentration in the hippocampus of resuscitation groups was significantly lower compared with preconditioning group 0-15min after ischemia (P<0.05).The recovery time of reverse reflection in the protective groups was shorter compared with preconditioning group after ischemia for 15 min (P<0.05). The viable neurons in the CA1 sector of the hippocampus of the protective groups were significantly higher compared with preconditioning group and resuscitation group after ischemia for 10 and 15 min (P<0.05). The apoptosis rates in the CA1 sector of the hippocampus of protective groups were significant lower than preconditioning group and resuscitation group after 10 and 15 min ischemia (P<0.05). Conclusions Isoflurane anesthesia could produce better improve global cerebral ischemia-reperfusion injury, but the protective effect of preconditioning and resuscitation appears to be similar.