Effect of dexmedetomidine on antioxidant ability in rats brain with focal cerebral ischemia/reperfusion
- VernacularTitle:右美托咪定对大鼠局灶性脑缺血-再灌注损伤后抗氧化能力的影响
- Author:
Chen LAN
;
Jiangbei CAO
- Publication Type:Journal Article
- Keywords:
Dexmedetomidine;
Reperfusion injury;
Antioxidant enzymes;
Brain
- From:
The Journal of Clinical Anesthesiology
2016;32(5):488-490
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effect of dexmedetomidine preconditioning on antioxidant ability in Rats Brain with focal cerebral ischemia/reperfusion.Methods Forty-two healthy male SD rats,weighted 250-280 g,were randomly divided into three groups (n = 14):sham-operation group (group Sham):in which carotid artery was exposed but MCAO was not performed;ischemia/reper-fusion group(group IR):NS were injected intraperitoneally at 30 minutes before the MCAO;dexme-detomidine group (group Dex):dexmedetomidine 100 μg/kg were injected intraperitioneally injected at 30 minutes before the MCAO.Focal cerebral ischemia-reperfusion (IR)model in rats was made by transient occlusion of the middle cerebral artery occlusion (MCAO)using a nylon thread with rounded tip inserted into internal carotid artery and advanced cranially until resistance was met.MCAO was maintained for 2 hours followed by 24 hours reperfusion.Neurologic deficit scores(NDS),the infarc-tion volume as well as the activities of endogenous antioxidants (such as superoxide dismutase(SOD), glutathione peroxidase(GSH-PX),glutathione reductase (GR),catalase (CAT))in ischemic brain were evaluated 24 h after reperfusion.Results Compared to group Sham,the neurologic deficit scores and the infarction volume in group Dex and IR were significantly higher,but the concentration of SOD,GSH-PX,GR,CAT were significantly lower(P <0.05).Compared to group IR,however,the neurologic deficit scores and the infarction volume in group Dex were significantly lower,but the concentra-tion of SOD,GSH-PX,GR,CAT were significantly higher (P <0.05).Conclusion Dexmedetomidine can protect the brain from focal cerebral ischemia-reperfusion injury,and its mechanism maybe relate to preserving the activities of endogenous antioxidants.
