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围生期新生儿缺氧缺血性脑损伤(hypoxic-ischemic brain damage,HIBD)是目前新生儿死亡和婴幼儿致残的主要原因,全球有23%新生儿死于该病,部分幸存者可发生脑性瘫痪、智力低下、癫痫等永久性脑损害。临床早期采取亚低温和重复注射小剂量的促红细胞生成素是目前治疗该病的较有效措施,但其能否改善远期预后仍然不为人知。这就迫切需要发展新的脑补救策略。动物实验表明,锂对HIBD具有潜在的神经保护效应,其作用机制已经受到广泛关注,下面就锂的神经保护作用机制作一综述。
Perinatal neonatal hypoxic-ischemic brain damage (HIBD) is the leading cause of neonatal death and infant disability. 23% of newborns worldwide die of the disease and some survivors may Occurrence of cerebral palsy, mental retardation, epilepsy and other permanent brain damage. Early clinical use of mild hypothermia and repeated injections of small doses of erythropoietin is currently more effective treatment of the disease, but whether it can improve the long-term prognosis is still unknown. This urgently needs to develop a new brain remedy strategy. Animal experiments show that lithium has a potential neuroprotective effect on HIBD, and its mechanism of action has received widespread attention. The mechanism of lithium neuroprotection is reviewed below.