角膜内皮细胞损伤后早期超微结构改变

Early ultrastructural changes of corneal endothelium in rabbits with endothelial injury

目的 :了解角膜内皮细胞损伤的超微结构特征及其临床意义。 方法 :对 2 0只成年灰兔进行定量角膜内皮细胞损伤 ,伤后定期进行眼部裂隙灯检查、角膜厚度及眼压测定 ,预期取角膜材料进行透射电镜和扫描电镜检查。 结果 :角膜内皮细胞损伤后 1天可见细胞膜破损 ,细胞肿胀 ,细胞器颗粒粗大 ;伤后 3天内皮细胞崩解 ,胞质脱落 ,胞核裸露 ;伤后 5天出现细胞缺损区 ,膜脂降解聚积而形成脂质球 ,附着于细胞缺损区 ,角膜上皮细胞间隙增宽 ;伤后 7天角膜内皮细胞移行修复细胞缺损区 ;伤后 9天后内皮细胞异形明显 ,上皮细胞出现变性。角膜混浊与角膜厚度呈正相关。眼压增高者角膜厚度增加 ,内皮细胞损伤加重。 结论 :超微结构检查结果提示 ,角膜内皮细胞受损后细胞崩解似乎是必然的结局。动态测定角膜厚度可以判断角膜内皮细胞损伤的程度。

Objectives: To observe ultrastructural changes of the corneal endothelium and to assess the significance of the changes after irrigation and aspiration(I/A) of the anterior chamber in rabbits Methods: Corneal thickness and intraocular tension were measured and the ultrastructure of corneal endothelium was observed in scheduling times following I/A Results:Obvious injury of the membrane structure of corneal endothelium was viewed with scanning electron microscope 1 day after injury. Transmission electron microscope revealed marked swelling of the organelles, increasing vacuoles in the cytoplasm and swelling, denuding, dissolving of the cellular nuclei 3 days after injury. The lipoballs resulted from aggregation of lipid in the cellular membrane adhered to the defect region of endothelium 5 days after injury. Scanning electron microscope displayed marked sign of migration of the corneal endothelium 7 days following injury. The corneal endothelium was heteromorphic and the degeneration of the epithelium occurred. The corneal thickness gradually increased and directly related to the degree of the corneal muddiness. The corneal thickness increased and the injury of endothelium aggravated when intraocular tension increased. Conclusions:The results of ultrastructural examination indicated that destruction of the corneal endothelium following injury seems to be a consequential sequel. Dynamic corneal thickness measurement contributes to the judgement of degree of corneal endothelium injury. Control of intraocular tension is one of the important methods for preventing secondary injury of the corneal endothelium.