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

目的观察右美托咪定预先处理对大鼠局灶性脑缺血-再灌注损伤后抗氧化能力的影响。方法健康雄性SD大鼠42只,体重250~280g,随机分为假手术组(Sham组)、缺血-再灌注组(IR组)和右美托咪定组(DEX组),每组14只。采用大脑中动脉线栓法制作大鼠局灶性脑缺血-再灌注损伤模型,具体方法为线栓法栓塞大脑中动脉2h后恢复再灌注。Sham组仅分离血管,不留置线栓;于大脑中动脉栓塞前30 min DEX组给予腹腔注射盐酸右美托咪定注射液100μg/kg(4μg/ml),IR组腹腔注射等量的生理盐水。三组均于再灌注24h后取8只大鼠进行神经功能评分,测定脑梗死体积;剩余6只大鼠取脑组织检测超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSHPX)、谷胱甘肽还原酶(GR)和过氧化氢酶(CAT)活性。结果 IR组和DEX组神经功能评分明显高于Sham组,脑梗死体积明显大于Sham组,SOD、GSH-PX、GR、CAT活性明显低于Sham组(P0.05);DEX组大鼠神经功能评分明显低于IR组,脑梗死体积明显小于IR组,SOD、GSH-PX、GR、CAT活性明显高于IR组(P0.05)。结论右美托咪定有保护内源性抗氧化酶活性作用,可能有助于减轻大鼠脑缺血-再灌注损伤。

Effect of dexmedetomidine on antioxidant ability in rats brain with focal cerebral ischemia/reperfusion

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.