Yoshioka H, Katsume Y
Jpn J Ophthalmol. 1982;26(4):397-409.
Experimental central serous chorioretinopathy was produced in a cynomolgus monkey. The sites of the outer blood retinal barrier coinciding with the spots of fluorescein leakage as confirmed by fluorescein angiography were examined by light and electron microscopy. Degeneration of a few retinal pigment epithelial cells was found, suggesting that the leakage of fluorescein into the subretinal space resulted from the disruption of the outer blood retinal barrier due to degeneration of the retinal pigment epithelial cells. Loss of the diaphragms or defects of damaged endothelial cells were observed in the inner surface of the choriocapillaris underneath these degenerated pigment epithelial cells. The region of these endothelial cell defects was covered with fibrin-platelet clots, and further, a considerable amount of fibrin existed within the Bruch's membrane. It is, thus, suggested that abnormal hyperpermeability of the choriocapillaris plays an important role in the pathogenetic development of this disease. Moreover, the results obtained in this study demonstrate that regional reparation of degenerated retinal pigment epithelial cells at the sites of fluorescein leakage will be initiated by rapid migration of surrounding normal retinal pigment epithelial cells in this experimental model.
在一只食蟹猴身上诱发了实验性中心性浆液性脉络膜视网膜病变。通过荧光素血管造影证实,与荧光素渗漏点一致的外血视网膜屏障部位,用光学显微镜和电子显微镜进行了检查。发现少数视网膜色素上皮细胞发生变性,提示荧光素渗漏到视网膜下间隙是由于视网膜色素上皮细胞变性导致外血视网膜屏障破坏所致。在这些变性色素上皮细胞下方的脉络膜毛细血管内表面观察到内皮细胞隔膜缺失或受损缺陷。这些内皮细胞缺陷区域覆盖有纤维蛋白-血小板凝块,此外,在布鲁赫膜内存在大量纤维蛋白。因此,提示脉络膜毛细血管异常高通透性在本病的发病机制中起重要作用。此外,本研究结果表明,在该实验模型中,荧光素渗漏部位变性视网膜色素上皮细胞的区域修复将由周围正常视网膜色素上皮细胞的快速迁移启动。