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七氟烷预处理对大鼠脑缺血再灌注损伤的保护作用 被引量:4

Protective effects of sevoflurane preconditioning on cerebral ischemia-reperfusion injury in rats
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摘要 目的探讨七氟烷预处理是否减轻脑缺血再灌注引起的神经细胞凋亡。方法36只雄性SD大鼠(250—300g),随机分为5组:对照组(n=12);缺血再灌注组(n=12),动物建立大脑中动脉阻断再灌注模型;七氟烷预处理组(n=12),动物接受七氟烷预处理后建立大脑中动脉阻断再灌注模型。采用HE染色和透射电镜观察大鼠缺血再灌注脑区神经元的凋亡情况、原位细胞凋亡检测法计数神经元凋亡密度、免疫印迹(Westernblot)检测缺血脑区半胱氨酸蛋白酶Caspase-3表达及活化。结果HE染色、电镜的结果均提示七氟烷预处理组神经元凋亡比缺血再灌注组少、凋亡程度轻;神经元凋亡密度对照组为(13.0±1.4)个/0.1mm^2、缺血再灌注组为(189.8±6.8)个/0.1mm^2、七氟烷预处理组为(110.5±4.3)+/0.1mm^2,两两比较,差异有统计学意义;缺血脑区Caspase-3前体及其20000切割片段含量的相对灰度值分别为16.7±3.0、76.1±3.4、51.2±3.1及8.2±2.3、59.0±6.3、31.2±5.4。结论七氟烷预处理可通过减轻脑缺血再灌注引起的神经细胞凋亡而产生保护作用。 Objective To investigate if sevoflurane preconditioning attenuate neuronal apoptosis induced by isehemia-reperfusion. Methods Thirty-six male SD rats weighing 250 - 300 g were randomly divided into three groups (n = 12 each) : control group (group C), isehemia-reperfusion group (group IR) (rats were established cerebral artery clamped and reperfusion model), sevoflurane preconditioning group (group S) (rats were established cerebral artery clamped and reperfusion model after 1 h 2.4% sevoflurane preconditioning). Apoptosis neurons were observed by Hematoxylin and Eosin (HE) staining and transmission electron microscope, TdT mediated Dutp nick end labeling(TUNEL) method was used to count apoptosis neurons density, fresh ischemic brain tissue was taken out, while Caspase-3 zymogen and 20000 segment were checked by Western blot. Results apoptosis neurons in group IR were more than ones in group S under HE staining and light microscope and transmission electron microscope, and apoptosis neurons density (cell number/0. 1 mm^2) by TUNEL staining : group C, 13.0± 1.4; group IR, 189. 8± 6. 8; group S, 110. 5 ±4. 3, the relative gray values of the contents of procaspase-3 and its 20 000 cleavage fragment were 16. 72 ±3. 0, 76. 1 ±3.4, 51.2 ±3.1 and 8. 2 ±2. 3, 59.0 ±6. 3, 31.2±5.4 respectively. Conclusions Sevoflnrane pretreatment can protect neuron on ischemia-reperfusion injury by attenuating neuronal apoptosis in rats.
出处 《中华医学杂志》 CAS CSCD 北大核心 2009年第41期2943-2945,共3页 National Medical Journal of China
关键词 缺血 再灌注损伤 七氟烷 Ischemia Reperfusion injury Brain Sevoflurane
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  • 1朱斌,叶铁虎.二氮嗪预先给药对原代培养大鼠海马神经元缺氧/复氧损伤的保护机制[J].中华麻醉学杂志,2005,25(9):678-681. 被引量:2
  • 2Wei HF, Baobin K, Wei WL, et al, Isoflurane and sevoflurane affect cell survival and BCL - 2/BAX ratio differently. Brain Research, 2005,1037 : 139-147.
  • 3Engelhard K, Werner C, Eberspacher E, et al. Sevoflurane and propofol ingluence the expression of apoptosis regulation proteins after cerebral ischemia and reperfusion in rats. Eur J Anesthesiol, 2004, 21:530-537.
  • 4Wise FL, Raizada MK, Sumners C. Desflurane and sevoflurane attenuate oxygen and glucose deprivation - induced neuronal cell death. Journal of Neurosurgieal Anesthesiology, 2003,15: 193-199.
  • 5Warner DS, Zhou J, Ramani R, et al. Reversible focal ischenfia in the rat: effects of halothane, isoflurane, and methohexital anesthesia. Journal of Cerebral Blood Flow and Metabolism, 1991,11:794-802.
  • 6Sano T, Drummond JC, Patel PM, et al. A comparison of the cerebral protective effects of isoflurane and mild hypothermia in a model of incomplete forebrain ischemia in the rat. Anesthesiology, 1992,76:221- 228.
  • 7Kushikata T, Hirota K, Kotani N, et al. Isoflurane increases norepinephine release in the rat preoptic area and the posterior hypothalamus in vivo and in vitro:Relevance to thermoregulation during anesthesia. Neuroscience, 2005,131:79-86.
  • 8David S, Warner MD, Claude MF, et al. Sevoflurane and halothane reduce focal ischemic brain damage in the rat. Anesthesiology, 1993, 79 : 985-992.
  • 9Werner C, Mollenberg O,Kochs E, et al. Sevoflurane improves neurological outcome after incomplete cerebral ischemia in rats. British Journal of Anaesthesia, 1995,75:756-760.
  • 10Payne RS, Ozan A, Norbert R, et al. Sevoflurane -induced preconditioning protects against cerebral ischemic neuronal damage in rats. Brain Research ,2005, 1034 : 147-152.

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  • 1邵建林,朱俊超,吴滨阳,王俊科,马虹.异氟醚、七氟醚和地氟醚预处理对脑缺血再灌注损伤大鼠海马CBS/H_2S、iNOS/NO和HO-1/CO的影响[J].中华麻醉学杂志,2006,26(10):907-910. 被引量:10
  • 2龚耀先.修订韦氏成人智力量表手册[M].长沙:湖南医学院出版社,1995:110-169.
  • 3Mullonkal CJ,Toledo-Pereyra LH. Akt in ischemia and reperfusion[J]. J Invest Surg, 2007,20(3) : 195-203.
  • 4Dhanasekaran A, Gruenloh SK, Buonaccorsi JN, et al. Multiple antiapop- totic targets of the PI3K-Akt survival pathway are activated by epoxye- icosatrienoic acids to protect cardiomyocytes from hypoxia/anoxia[J]. Am J Physiol Heart Circ Physiol, 2008,294 (2) : 724-735.
  • 5Fujio Y, Nguyen T, Wencker D, eta|. Akt promotes survival of cardiomy- ocytes in vitro and protects against ischemia-reperfusion injury in mouse heart[J]. Circulation, 2000,101 ( 6 ) : 660-667.
  • 6Wang JK, Yu LN ,Zhang FJ ,et al. Postconditioning with sevoflurane pro- tects against focal cerebral ischemia and reperfusion injury via PI3K/Akt pathway[J]. Brain Res, 2010,1357 : 142-151.
  • 7Inamura Y,Miyamae M,Sugioka S,et al. Sevoflurane postconditioning prevents activation of caspase 3 and 9 through antiapoptotic signaling after myocardial ischemia-reperfusion[J]. J Anesth, 2010,24 (2) : 215-224.
  • 8DhanasekaranA,GruenlohSK,BuonaccorsiJN,etal.MultipleantiapoptotictargetsofthePI3KAktsurvivalpathwayareactivatedbyepoxyeicosatrienoicacidstoprotectcardiomyocytesfromhypoxia/anoxia[J].AmJPhysiolHeartCircPhysiol,2008,294(2):724-735.
  • 9YeZ,GuoQ,WangN,etal.DelayedneuroprotectioninducedbysevofluraneviaopeningmitochondrialATP-sensitivepotassiumchannelsandp38-MAPK-phosphorylation[J].NeurologicalSciences,2011,33(2):239-249.
  • 10ZhaoH,SapolskyRM,SteinbergGK,etal.Interruptingreperfusionasastroketherapy:Ischemicpostconditioningreducesinfarctsizeafterfocalischemiainrats[J].JCerebBloodFlow-Metab,2006,26:1114-1121.

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