| 1 | 大鼠视网膜缺血再灌注模型的建立与观察显示文摘目的观察视网膜缺血再灌注后视网膜的病理变化过程,探讨建立视网膜缺血再灌注动物模型的理想方法。方法成年Wistar大鼠30只,其中5只作为对照组外,余25只作为实验组。实验组再分为缺血6h、24h、48h、72h、7d组,每组5只。用自制升眼压装置,提高眼内压至125mmHg,持续60min造成视网膜缺血,之后解除压力。高眼压下观察眼结膜和眼底变化。缺血再灌注6h、24h、48h、72h、7d后摘除眼球,取视网膜进行组织学观察。结果高眼压下大鼠球结膜变苍白,视网膜苍白、水肿;解除高眼压后,可见球结膜充血,视网膜恢复血供。视网膜缺血再灌注后,视细胞外节肿胀、疏松、空泡化,内外核层细胞部分缺失,RGCs数目明显减少。结论高眼压法制造的视网膜缺血再灌注模型接近视网膜缺血临床病理过程,模型稳定、可靠。 | 程辉 李秀云 鞠学红 | 2009 | 解剖学研究2009，31，2： | 11 |
| 3 | Pathological changes in the retina and growth associated protein-43 expression following treatment of intracanalicular optic nerve injury via optic canal decompression,dexamethasone or their combination显示文摘BACKGROUND:The main clinical treatments for optic nerve injury are optic canal decompression and systemic administration of hormones,but both treatments have disadvantages.OBJECTIVE:To observe the pathological changes in the retina and growth associated protein-43(GAP-43) expression,to compare the treatment of optic canal decompression,hormones,and their combination with the intracanalicular optic nerve injury.DESIGN,TIME AND SETTING:A randomized,controlled animal study was performed at the Department of Anatomy,Weifang Medical University,China,from September 2007 to November 2008.MATERIALS:Dexamethasone(Shandong Huaxin Pharmaceutical,China) and rabbit anti-GAP-43 polyclonal antibody(Boster,China) were used.METHODS:All 36 healthy adult rabbits were randomly assigned to control group(n = 4),simple injury group(n = 20),and treatment group(n = 12).Intracanalicular optic nerve injury models were established using the metal cylinder free-fall impact method.The control group was left intact.The treatment group(four rabbits in each subgroup) was treated by optic nerve decompression,dexamethasone treatment(1 mg/kg daily via two intravenous infusions,1/5 total dose reduction every 3 days,for 14 days),and simultaneously giving surgery and hormone treatment.MAIN OUTCOME MEASURES:Pathological changes in the retina were determined using hematoxylin-eosin staining.GAP-43 expression was detected using immunohistochemistry in the retina.RESULTS:Retina injury induced obvious pathological changes in the retina.With prolonged time after optic nerve injury,the number of retinal ganglion cells was gradually decreased,and reached the minimum on day 14(P < 0.01).All three treatments increased the number of retinal ganglion cells(P < 0.01),but surgery + hormone treatment was most effective.No GAP-43 cells were present in the normal retinal,but they appeared 3 days after injury,peaked 7 days after injury,and then began to decline.CONCLUSION:Intracanalicular optic nerve injury induced obvious pathological changes in the retina,including increased GAP-43 expression.Optic canal decompression and hormones improved nerve repair after injury,and their combination produced better outcomes. | Xuehong Ju Hui Cheng Hongguo Liu Xiaoshuang Li Xiuyun Li | 2010 | Neural Regeneration Research2010，5，10： | 2 |
您所在的机构暂未开通此部分的功能，请联系管理员