摘要
目的观察七氟醚后处理对大鼠海马脑片缺氧无糖损伤保护与线粒体ATP敏感性钾通道(mitochondfiMATP.sensitivepotassiumchannels,mitOKATp)的关系。方法将符合标准的海马脑片按随机数字表法分为4组(每组10片):缺氧无糖损伤对照组(oxygenglucosedeprivation,OGD组)、4%七氟醚(sevoflurane)后处理组(4%Sevo组)、mitoKATP通道阻滞剂5-羟葵酸盐(5-hydmxvdeeanoate,5-HD)组(5-HD组)、4%七氟醚后处理+5-HD组(SHD组),采用脑片灌流及电生理技术,细胞外记录海马CAl区的顺向群锋电位(orthodromicpopulationspike,OPS);利用2,3,5-三苯基氯化四氮唑(2,3,5-triphenyltetrazoliumchloride,TYC)染色定量比色方法分析脑片损伤程度。结果与OGD组比较,4%Sevo组OPS恢复程度(68±9)%和恢复率(60%)升高,组织损伤百分率(0.40±0.05)降低。与4%Sevo组比较,5-HD组和SHD组OPS恢复程度(6±5)%、(7±7)%和恢复率(10%、20%)降低,组织损伤百分率(0.64±0.08、0.65±0.06)升高。结论七氟醚后处理可减轻大鼠海马脑片缺氧无糖损伤,该保护作用与mitoKAav通道的激活有关。
Objective To examine whether the activation of mitochondrial ATP-sensitive potassium channels (mitoKATO) ehannals is involved in the neuroproteetive effect of sevoflurane postconditioning against oxygen-glucose deprivation (OGD) injury in rat hippoeampal slices. Methods Forty hippocampal slices were randomly divided into 4 groups (n=10 each): OGD group; 4% Sevo group; 5-HD group and 4% Sevo +5-HD group. By electrophysiological recording technique, orthodromic population spike (OPS) in the stratum pyramidale of the CA1 region were measured. And TTC staining was used to calculate the percentage of tissue injury. Results In Sevo group the degree (68±9)% and rate of recovery (60%) of OPS were increased and the percentage of tissue injury (0.40±0.05) was decreased as compared with OGD group. While in HD group and SlID group the degree (6±5)%, (7±7)% and rate of recovery (10%,20%) of OPS were decreased and the percentage of tissue.injury (0.64±0.08,0.65±0.06) was increased as compared with Sevo group. Conclusions Sevoflurane postconditioning can attenuate the OGD injury to rat hippocampal slices. The activation of mitoKATP channals is involved in the protective effect of sevoflurane postconditioning against OGD injury.
出处
《国际麻醉学与复苏杂志》
CAS
2012年第12期798-800,共3页
International Journal of Anesthesiology and Resuscitation
关键词
线粒体ATP敏感性钾通道
七氟醚后处理
海马脑片
缺氧无糖损伤
mitochondrial ATP -sensitive potassium channels
Sevoflurane postconditioning
Hippocampal slices
Oxygen-glucose deprivation injury