谷氨酸在心肺脑复苏中的影响

The Effect of Glutamic Acid in Cardiopulmonary-cereal Resuscitation

心跳呼吸骤停及心肺脑复苏(CPCR)的过程均导致机体发生缺血/再灌注损伤(I/R)等复杂的病理生理变化。脑的缺血再灌注损伤是一个快速的级联反应,包括能量代谢障碍、氧自由基的生成增多、兴奋性氨基酸释放增加、炎性细胞因子释放增加等。这些环节紧密连接,互为因果,形成恶性循环,最终导致神经元的凋亡或坏死。谷氨酸是大脑中一种关键的兴奋性神经递质,它的过多释放在神经元损伤发展过程中起着重要作用。随着细胞外高浓度谷氨酸的结合,N-甲基-D-天冬氨酸受体(NMDAR)开放,大量Ca2+内流,导致细胞内钙超载,是引起脑损伤的共同通路。本文就神经兴奋毒性的研究进行综述。

Cardiac arrest and cardiopulmonary-cereal resuscitation（CPCR） may induce complicated pathophysiological changes of ischemia/reperfusion injury.Cerebral ischemia/reperfusion injury is a rapid cascade process,including dysmetabolism of energy,ex-cessive released of oxygen free radicals,excitatory aminoacids and inflammatory cytokines.These are closely linked to each other,cause and effect,form a vicious cycle leading to neuron apoptosis or necrosis.Glutamic acid（Glu） is a key excitatory neurotransmitter in the brain,and its excessive release plays a key role in the development of neuronal injury.Generally,N-methyl-D-aspartate receptor（NM-DAR） opening following extracellular high concentration glutamic acid binging,great Ca2＋ influx through the receptors,lead to intracel-lular calcium overload,is a common pathways of brain damage.This paper reviewed the neuronal excited toxicity.