Korte G E, Reppucci V, Henkind P
Invest Ophthalmol Vis Sci. 1984 Oct;25(10):1135-45.
The authors have obtained evidence that destruction of the retinal pigment epithelium (RPE) causes choriocapillaris (CC) atrophy. The observations led us to hypothesize that the RPE modulates CC structure and function. Rabbits received injections of sodium iodate, which selectively destroyed the RPE. The authors killed the rabbits at various times after iodate and examined the RPE and CC by fluorescein angiography, fundus photography, and light and electron microscopy. Fluorescein angiography and fundus photography revealed a pattern of retinopathy similar to that described by other investigators, eg, blood-retinal barrier breakdown and the patchy nature of the RPE/CC degeneration. One week after injection of iodate, the RPE transformed into a mixture of flattened, depigmented cells and plump, highly pigmented ones lying along Bruch's membrane. The CC appeared normal by light microscopy, but electron microscopy revealed changes indicating CC atrophy: degenerating endothelial cells (EC), EC that appeared normal but had reduced numbers of fenestrae, and pericapillary basal laminae that looped away from the endothelium, as if the latter had shrunk. One month after iodate, patches of Bruch's membrane were devoid of RPE, which was replaced by scar tissue. The CC was markedly atrophic over these patches, having reduced numbers of profiles and smaller lumina in those which remained. The CC appeared normal over areas where RPE remained. Eleven weeks after iodate, the light microscopic picture parallelled that seen 1 month after injection, but the patchy RPE degeneration was more extensive. By electron microscopy, the CC profiles over areas devoid of RPE showed severe atrophy. Degenerating EC were more numerous. EC adjacent to areas of RPE loss had few or no fenestrae. Here, capillaries were encased in dense, collagenous, connective tissue, unlike the CC of normal rabbits. These changes were not seen where the RPE still covered Bruch's membrane. These observations suggest that RPE modulates CC structure and function. The authors propose that a diffusible vascular modulating factor produced by RPE cells does this.
作者已获得证据表明,视网膜色素上皮(RPE)的破坏会导致脉络膜毛细血管(CC)萎缩。这些观察结果使我们推测,RPE调节CC的结构和功能。给兔子注射碘酸钠,其可选择性地破坏RPE。作者在注射碘酸钠后的不同时间处死兔子,并通过荧光素血管造影、眼底照相以及光镜和电镜检查RPE和CC。荧光素血管造影和眼底照相显示出一种视网膜病变模式,类似于其他研究者所描述的,例如血视网膜屏障破坏以及RPE/CC变性的斑片状性质。注射碘酸钠一周后,RPE转变为扁平、色素脱失细胞与沿布鲁赫膜排列的饱满、色素高度沉着细胞的混合物。光镜下CC看似正常,但电镜显示出表明CC萎缩的变化:内皮细胞(EC)退变、看似正常但窗孔数量减少的EC以及从内皮细胞处呈环状离开的毛细血管周围基膜,就好像内皮细胞已经萎缩。注射碘酸钠一个月后,布鲁赫膜的一些区域没有RPE,取而代之的是瘢痕组织。这些区域的CC明显萎缩,剩余的CC轮廓数量减少且管腔变小。RPE留存区域的CC看似正常。注射碘酸钠十一周后,光镜图像与注射后1个月时所见相似,但斑片状RPE变性更为广泛。通过电镜观察,无RPE区域的CC轮廓显示出严重萎缩。退变的EC更多。与RPE缺失区域相邻的EC几乎没有或没有窗孔。此处,毛细血管被致密的胶原结缔组织包裹,这与正常兔子的CC不同。在RPE仍覆盖布鲁赫膜的地方未见到这些变化。这些观察结果表明,RPE调节CC的结构和功能。作者提出,RPE细胞产生的一种可扩散的血管调节因子发挥了这一作用。