摘要
背景围术期缺血性脑损伤的发生会造成灾难性后果。在体和离体实验发现七氟烷预处理能够改善缺血性脑损伤。然而,其神经保护作用的分子机制尚未完全阐明。目的探讨七氟烷预处理的神经保护机制。内容现从七氟烷预处理对线粒体ATP敏感性钾通道(mitochondrial ATP-sensitive potassium channel, mitoKATp)的激活、兴奋性毒素应激因子的减少、抑制凋亡与炎症等方面的机制研究进展进行综述。趋向七氟烷预处理可能通过多位点和多途径交互作用来发挥神经保护作用。
Background Peri-operative cerebral ischemia can be catastrophic. In vivo and in vitro studies have demonstrated that sevoflurane preconditioning is able to protect brain against isehemic injury. However, its molecular mechanisms are far from clearly elucidated. Objective In this review, we will introduce the neuroprotective mechanisms of sevoflurane preconditioning. Content This paper reviewed proposed mechanisms including activation of ATP-sensitive potassium channels, reduction of excitotoxic stressors, up-regulation of anti-apoptotic factors and down-regulation of proinflammatory cytokines. Trend Sevoflurane preconditioning may contribute its neuroprotective effects to the interaction of multi-targets and multi-pathways.
出处
《国际麻醉学与复苏杂志》
CAS
2011年第1期117-120,共4页
International Journal of Anesthesiology and Resuscitation
基金
资助基金:同家自然科学基金面上项目(30772079、30870794)
复旦大学脑科学研究院开放研究课题基金
复旦大学附属华山医院科研启动基金
贝朗麻醉科学研究基金
关键词
七氟烷
预处理
脑缺血
再灌注损伤
Sevoflurane
Preconditioning
Cerebral ischemia
Reperfusion injury