谷氨酸与缺血性卒中早期神经功能恶化

Glutamate and early neurological deterioration in ischemic stroke

缺血性卒中早期神经功能恶化（early neurological deterioration，END）的机制尚不明确，也缺乏可靠的预测因素和有效的防治措施。谷氨酸介导的兴奋性毒性机制在缺血事件级联反应中发挥着很重要的作用。血浆谷氨酸水平增高是END的重要预测因素之一。研究表明，兴奋性氨基酸转运体一2基因启动子区多态性是个体对END易感性的潜在原因。一些拈抗谷氨酸能通路的治疗策略可作为干预END的策略。

The mechanisms underlying early neurological deterioration （END） after ischemic stroke are not clear. There are no reliable predictive factors and effective preventive measures for END. The glutamate-mediated excitotoxicity plays a very important role in the cascade reaction of ischemic events. High level of glutamate in plasma is one of the important predictors for END. Studies have shown that the polymorphism in the promoter of the excitatory amino acid transporter-2 gene is a potential cause for individual susceptibility to END. Some therapeutic strategies of interrupting the glutamatergic pathways may be as the strategies of intervention END.