高氧诱导眼损伤机制及其防治的研究进展  

Current progress in pathogenesis and prevention of hyperoxia-induced ocular injury

作　　者：李琪（综述）[1] 严宏（审校）[1] 

机构地区：[1]第四军医大学唐都医院眼科,西安710038

出　　处：《中华实验眼科杂志》2011年第2期184-187,共4页Chinese Journal Of Experimental Ophthalmology

基　　金：国家自然科学基金项目（30872837）

摘　　要：高氧包括高压氧和高浓度氧，在多种眼科疾病的治疗中发挥重要作用，如视网膜静脉阻塞、缺血性视神经病变、中心性浆液性脉络膜视网膜病变等。但是，长时间吸入的氧气浓度过高或压力过大可导致眼部组织损伤，其中晶状体混浊、早产儿视网膜病变、近视是应用高氧治疗后较常见的眼部并发症。目前，高氧性眼损伤的发病机制尚未完全明确，许多学者认为其发生与氧化应激、脂质过氧化反应、炎性反应等多种因素有关。就高氧对晶状体和视网膜等眼内组织损伤机制及其防治措施的最新研究进展进行综述。Hyperoxia,including hyperbaric oxygen （HBO） and high-concentration oxygen （HO）, has an important therapeutic effect on various ophthalmological diseases, such as retinal vein occlusion, ischemic optic neuropathy and central serous chorioretinopathy. However,excessive inhalation of oxygen of high-concentration or high atmospheric pressure can cause damage of ocular tissue, in which the lens opacity and retinopathy of prematurity （ROP） are the most common complications following hyperoxia exposure. At present,the pathogenesis of hyperoxia- induced ocular injury is still unclear thoroughly, and it may be related to oxidative stress, lipid peroxidation and inflammation. This article reviewed the current advance in the mechanism and the potential prevention of hyperoxia- induced the lens, retina and other ocular injuries.

关 键 词：高氧 氧化应激 脂质过氧化 晶状体 视网膜 

分 类 号：R774.02[医药卫生—眼科]