摘要
目的 :研究一氧化氮在短暂高眼压诱导的视网膜缺血性损伤的作用机制。方法 :48只雄性S -D大鼠随机分为两组 ,每组 2 4只。 1组左眼为正常对照组、右眼为视网膜缺血对照组 ;2组左眼为视网膜缺血溶剂对照组 ,右眼为视网膜缺血L -NAME治疗组。视网膜缺血再灌注后 7、 14、 2 8天分别将各组 2 4只眼随机分入 3个时间点 ,每个时间点 8只眼。制备视网膜病理切片 ,定量测量内网状层 (IPL)、内核层 (INL)、外核层 (ONL)的厚度。结果 :在缺血的早期阶段 (第 1周 ) ,内网状层 (IPL)的厚度即下降 ,在缺血的晚期阶段 (第 2周～第 4周 ) ,内核层 (INL)和外核层 (ONL)的厚度才发生显著下降。与对照组相比差异均有显著性 ( χ2 检验 ,P <0 0 5 )。L -NAME ,一氧化氮合酶抑制剂可明显减轻缺血性损伤。减轻视网膜各层的下降幅度。与缺血对照组相比经统计学处理差异均有显著性 ( χ2 检验 ,P <0 0 5 )。结论 :视网膜缺血性损伤的诱导机制除了兴奋性毒性诱导的损伤以外 ,还有其他的机制存在。NO可介导视网膜缺血性损伤 ,并在短暂视网膜缺血后晚期内核层 (INL)与外核层 (ONL)神经元的延迟死亡起到一个主要的作用。
Purposes:To investigate the role of nitric oxide(NO) in the rat retina following ischemic injury induced by transient increase of intraocular pressure. Methods:Forty eight male S-D rats are randomly divided into two groups,twenty four rats in every group,twenty four rats in the first group under anesthesia were subjected to one hour of complete ischemia in the right eyes by raising the intraocular pressure,the left eye in each animal served as a normal control,twenty four rats in the second group received one intravitreal injection of the veicle in the left eyes one hour after cessation of ischemia,the right eye in each animal of this group received one intravitreal injection of L NAME.24 eyes in every group were respectively divided into 3 time points randomly at the sevent day,the fourteenth day and the twenty eighth day after ischemia.Ischemic damage and protection of L NAME of IPL?INL and ONL were histologically quantified at every time point. Results:The thickness of the inner plexiform layer(IPL) decreased during early postischemic stages(up to one week).In late postischemic stages(two four weeks),the thickness of the inner nuclear layer and the outer nuclear layer decreased markedly.Significant statistical differences were found between the control group and the ischemic group(P<0 05).Treatment of rats with N G nitro L arginine methyl ester(L NAME),a nitric oxide synthase(NOS)inhibitor,significantly reduced ischemic damage.L NAME Treatment reduced the magnitude of the retinal thickness decrease.Significant statistical differences were found between the L NAME treatmet group and the ischemic grioup(P<0 05). Conclusions:NO is involved in the mechanism of ischemic injury and plays a key role in the delayed and sustained cell death in the ONL following transient retinal ischemia.
出处
《中国实用眼科杂志》
CSCD
北大核心
2003年第6期474-477,共4页
Chinese Journal of Practical Ophthalmology
