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作 者:陈少军[1] 阴正勤[1] 李世迎[1] 王仕军[1]
出 处:《眼科研究》2008年第10期735-738,共4页Chinese Ophthalmic Research
摘 要:目的通过持续光照建立大型动物的慢性视网膜变性模型,用于视网膜移植实验研究。方法利用可见光持续照射12只2月龄猪达3个月以上,慢性诱导微型猪视网膜变性。采用多焦视网膜电图检测正常猪及光性视网膜变性猪N1和P1波振幅和潜伏期,比较各观察值的变化;用光镜、电镜观察其视网膜外核层厚度变化及细胞器超微结构状况,从形态和功能两方面对光损伤模型进行鉴定。结果同正常猪比较,光性视网膜变性猪N1、P1波振幅在1-6环内均明显降低,而在视网膜内传导时间明显延长;苏木精-伊红染色光镜下见感光细胞内外节变短,外核层细胞核减少至4-6排,外核层厚度减少了20.98%;电镜下可见后极部感光细胞线粒体肿胀明显、嵴断裂、数量减少。结论微型猪光性视网膜变性模型经功能和形态两方面鉴定光损伤部位是在光感受器,建立用于视网膜移植实验的大型动物模型获得成功。Objective Many animal models have been used in retinal degeneration study.However,a suitable model of retinal degeneration for retinal surgery and transplantation mimicking human retinal degeneration is still underinvestigation.Therefore,this study was to establish and offer a slow photoreceptor degeneration model in animal for the experimental study of retinal transplantation.MethodsTwelve adult miniature pigs aged 2 months were exposed constantly to the visible light with the spectrum 400-700nm,intensity 2500 Lx and irradiating 12 hours per day for more than 3 months to induce slowly retinal degeneration;2 normal pigs were as control.The amplitude and latency of N1,P1 waves of mfERG were recorded in light-induced group and normal group,and the thickness change of retinal outer nuclear layer (ONL) and organelle ultrastructure was observed under the light microscope and electron microscopy in both groups.ResultsCompared with the normal control,the amplitudes of N1,P1 waves were lower obviously from 1 ring to 6 rings(P〈0.05-0.01),and the mean latencies of N1 and P1 waves in various rings were extended obviously in the light-induced retinosis (P〈0.05-0.01).The photoreceptor cells were manifested as shortening of outer segments and reduction of cells in the ONL,and the thicknesses of the ONL decreased to 20.98%.The edema of mitochondria of photoreceptor cells was seen and followed the rupture of crista and the reduction of quantity by means of the electron microscope.ConclusionThe model of light-induced retinal degeneration is successfully created in the miniature pig by exposure of visible light and verified by function and modality as follows:the light damage locates in photoreceptor cells and shows a mfERG abnormality.This manifestation is similar to the process of mankind slow photoreceptor degeneration.
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