摘要
视网膜缺血损害的机制复杂,大量的研究资料表明视网膜在缺血及再灌注时谷氨酸的释放量增加,谷氨酸的兴奋性毒性作用在缺血视网膜的病理发展中起到了重要的作用,是引起缺血视网膜神经元死亡的重要因素。通过减少谷氨酸的释放,应用谷氨酸受体拮抗剂限制谷氨酸的生物活性等,可以阻止或减轻缺血视网膜的损害。虽然到目前为止临床上还未出现治疗视网膜缺血的有效药物,但对谷氨酸的损害机制和相关治疗策略的实验性研究,为治疗该疾病提供了广阔的前景。
The mechanism of glutamate on retinal ischemia is very complicated. Many investigations have suggested that the glutamate releases increased in retina during the stage of retinal ischemia and reperfusion. It has been strongly implicated that the excitotoxicity of glutamate plays an important role in the pathogenesis of retinal ischemia, which results in ischemic neuronal death. This can be prevented or reduced by decreasing the release of glutamate as well as limiting its bioactivity by using some glutamate receptor antagonist. Though the drug to effectively treat retinal ischemia is not available currently in clinical trial, the experimental study on mechanisms of the damage of glutamate on retinal ischemia and relative therapeutic strategies brings light to the treatment of retinal ischemia.
出处
《国际眼科杂志》
CAS
2005年第5期1006-1009,共4页
International Eye Science
基金
中国军队医药卫生科研基金项目(No.01MA197)
