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新生儿缺氧缺血性脑病(HIE)是一种严重威胁新生儿生命并可导致严重后遗症的疾病,病死率较高。近年来,已认识脑缺氧缺血均可引发和催化脑组织中病理性自由基瓜增强而产生大量自由基,自由基加剧脑血管痉挛,使毛细血管通透性增高及血管内微血栓形成。为清除体内产生的自由基,SOD大量消耗,致使体内SOD减少。文献资料表明,即使轻度HIE时,血中SOD即明显降低,LPO增多,提示新生儿HIE时血中自由基增多,自由基大量产生及由此引起的脂质过氧化反应,参与并加重了缺氧缺血所致的脑组织损害,是HIE发病机理之一。
Neonatal hypoxic-ischemic encephalopathy (HIE) is a disease that poses a serious threat to the life of newborns and can lead to serious sequelae with a high case fatality rate. In recent years, it has been recognized that hypoxic-ischemic brain can induce and catalyze the increase of pathogenic free radicals in brain tissue to produce a large number of free radicals, which aggravate cerebral vasospasm, increase capillary permeability and microvascular thrombosis . To clear the body of free radicals, SOD consumption, resulting in reduced body SOD. Literature data shows that, even mild HIE, SOD was significantly lower blood, LPO increased, suggesting that newborn blood HIE increased free radicals, a large number of free radicals and lipid peroxidation caused by the participation and aggravate Hypoxic-ischemic brain damage caused by one of the pathogenesis of HIE.