摘要
背景临床上蛛网膜下腔出血、重度脑损伤、脑梗死、失血性休克等患者救治过程中均可发生脑缺血／再灌注损伤（cerebral ischemia/reperfusion injury, CI/RI ）。七氟醚后处理作为一种在时序上与这种病理生理过程一致、具有潜在脑保护临床价值的新方法，近年来受到广泛的关注。目的对七氟醚后处理改善CI／RI的机制进行综述。内容七氟醚后处理减轻CI／RI涉及磷脂酰肌醇3-激酶/蛋白激酶B（phosphatidylinositol 3-kinase and protein kinase B, PI3K/Akt）、氧化应激、线粒体ATP敏感钾通道（mitochondrial ATP-sensitive potassium channel, mito KATP）、线粒体膜通透性转运孔 （ mitochondrial permeabilitytransition pore, mPTP）、细胞外信号调节激酶1/2（extracellular signaling-regulated kinase 1/2, ERK1/2）等途径。趋向通过了解七氟醚后处理减轻CI／RI的机制，为更好地治疗CI／RI提供理论依据。
Background Cerebral ischemia/reperfusion injury （CI/RI） may be occur in the patients during subarachnoid hemorrhage, severe brain injury, cerebral infarction and hemorrhagic shock. Sevoflurane postconditioning which is in accordance with the pathophysiologic process in timing sequence and as a novel method of potential value .for cerebral protection, have attracted extensive attention in recent years. Objective This paper reviewed the mechanisms of sevoflurane postconditioning against CURl. Content Phosphatidylinositol 3-kinase, protein kinase （PI3K/Akt）, oxidativestress, mitochondrial ATP-sensitive potassium channel （mitoKATP）, mitochondrial permeability transition pore （mPTP）, extracellular signaling-regulated kinase 1/2 （ERKI/2） are involved in neuroproteetion by sevoflurane postconditioning under the setting of CI/RI. Trend To understand the mechanisms of sevoflurane postconditioning against CI/RI, and provide a theoretical basis for better treatment of CUR1.
出处
《国际麻醉学与复苏杂志》
CAS
2017年第3期243-247,共5页
International Journal of Anesthesiology and Resuscitation
基金
国家自然科学基金（81471341）
安徽省自然科学基金（1508085MH184）
关键词
七氟醚
后处理
脑
缺血
再灌注损伤
保护机制
Sevoflurane
Postconditioning
Cerebral
Ischemia/reperfusion injury
Protection mechanism
