RESUMEN
Objective To investigate the protective effect of sevoflurane on the brain against focal ischemia-reperfusion(I/R)injury and its mechanism.Methods Twenty-four male SD rats weighing 250-300 g were randomly allocated into 3 groups(n=8 each):group Ⅰ sham operation;grouop Ⅱ I/R and group Ⅲ I/R + sevoflurane.The rats were anesthetized with intraperitoneal chloral hydrate 300 mg?kg~(-1).Middle cerebral artery occlusion(MCAO)was produced by insertion of a 4-0 mono-filament nylon thread with rounded tip at bifurcation of right common carotid artery into internal carotid artery.The nylon thread was advanced cranially until resistance was felt.The depth of insertion was 18-20 mm.After 3 h MCAO the thread was withdrawn to allow reperfusion.In group Ⅲ the animals inhaled 1.0 MAC sevoflurane for 30 min at 30 min before reperfusion.The rectal temperature of the animals was kept at 36.5-37.5℃.At the end of 24 h reperfusion the animals were weighed again.The animals'neurological deficit was evaluated using Zea Longa score(0=no defcit,4=unable to walk and unconscious).The animals were then killed.The neuronal apoptosis in striatum was assessed(TUNEL)and the PKC protein expression in striatum was determined by immunocyto-chemistry.Results The body weight of the animals in I/R group was significantly reduced after 24h reperfusion as compared to the body weight before ischemia (P＜0.01),while in control group and sevoflurane group there was no significant difference in the body weight before and after sham operation or I/R.The neurological deficit scores were significantly higher in I/R group than in sevoflurane group.The number of apoptotic neurons in striatum was significantly higher in I/R group than in sevoflurane group.The PKC expression in striatum was significantly higher in sevoflurane group than in I/R group (P＜0.01).Conclusion 1.0 MAC sevoflurane inhalation has protective effect on the brain against I/R injury. Upregulation of PKC expression in striatum decreased by I/R is involved in the mechanism.