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Macular hole retinal detachment in highly myopic eyes: ultrastructure of surgically removed epiretinal membrane and clinicopathologic correlation.

机译:近视眼黄斑裂孔视网膜脱离:手术切除的视网膜前膜的超微结构和临床病理相关性。

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PURPOSE: To elucidate the pathogenesis of macular hole retinal detachment (RD) in highly myopic eyes by investigating the ultrastructure of surgically removed epiretinal membranes (ERM). METHODS: Five consecutive Japanese patients with macular hole RD in highly myopic eyes underwent vitrectomy with attempted removal of the ERM around the hole. The surgical specimens were examined by light microscopy and by scanning and transmission electron microscopy. RESULTS: Extremely thin, translucent sheets of epiretinal tissue were harvested from all patients during surgery, resulting in successful retinal reattachment. Ultrastructural examination revealed that the ERM consisted of cortical vitreous and various cellular components. Fibrous astrocytes were the major cell population and extended cytoplasmic processes with membrane-associated vesicles onto the cortical vitreous. Gap junctions were observed between the interdigitating processes of fibrous astrocytes. The cortical vitreous contained abundant newly formed collagen, including fibrous long-spacing collagen, surrounded by sparsely distributed native vitreous collagen. CONCLUSIONS: Active synthesis of new collagen may be regulated by fibrous astrocytes by means of transmission of metabolic substances through gap junctions and cytoplasmic vesicles. The frequent occurrence of newly formed collagen aggregates may subsequently lead to a diffusely condensed posterior cortical vitreous that exerts tangential traction on the posterior retina, causing macular hole RD.
机译:目的:通过研究手术切除的视网膜前膜(ERM)的超微结构,阐明高度近视眼中黄斑裂孔视网膜脱离(RD)的发病机理。方法:连续五名日本近视眼的黄斑裂孔性视网膜病变患者接受了玻璃体切除术,并试图切除了裂孔周围的ERM。通过光学显微镜以及扫描和透射电子显微镜检查手术标本。结果:在手术过程中,所有患者均收获了非常薄的半透明的视网膜前组织片,从而成功地使视网膜复位。超微结构检查显示,ERM由玻璃体皮质和各种细胞成分组成。纤维状星形胶质细胞是主要的细胞群,其胞质过程与膜相关囊泡扩展到皮质玻璃体上。在纤维状星形胶质细胞的交叉指指过程之间观察到间隙连接。皮质玻璃体包含丰富的新形成的胶原蛋白,包括纤维状长间隔胶原蛋白,周围分布着稀疏的天然玻璃体胶原蛋白。结论:纤维状星形胶质细胞可以通过间隙连接和胞质囊泡代谢新陈代谢物质来调节新胶原的主动合成。新形成的胶原蛋白聚集体的频繁出现可能随后导致后部皮质玻璃体的弥散浓缩,在后部视网膜上施加切向牵引力,引起黄斑裂孔RD。

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