Glatt H, Machemer R
Am J Ophthalmol. 1982 Dec;94(6):762-73. doi: 10.1016/0002-9394(82)90301-4.
In order to simulate the hemorrhagic detachment stage of disciform macular degeneration, we injected fresh autologous blood into the subretinal space of albino rabbits and studied these hemorrhages clinically with the ophthalmoscope and by light and electron microscopy. One hour after injection, retinal changes were minimal and limited to occasional photoreceptor edema. At one day, there was marked damage of the photoreceptor cells characterized by edema and disintegration of the photoreceptors and pyknosis of the outer nuclear layer. Some photoreceptors had been pulled off the retina by contraction or movement of the blood clot, or both. By seven days, the photoreceptor cells were almost absent. Subretinal hemorrhage in rabbits led to irreversible retinal destruction within 24 hours. We think that the mechanism of the destruction of the overlying retina consists of a combination of a diffusion barrier by the clot, mechanical damage to the outer segments by contraction of the clot, and iron toxicity.
为了模拟盘状黄斑变性的出血性脱离阶段,我们将新鲜自体血注入白化兔的视网膜下间隙,并通过检眼镜以及光镜和电镜对这些出血进行临床研究。注射后1小时,视网膜变化极小,仅限于偶尔的光感受器水肿。1天时,光感受器细胞出现明显损伤,表现为光感受器水肿、崩解以及外核层固缩。一些光感受器因血凝块的收缩或移动,或两者共同作用而从视网膜上脱落。到7天时,光感受器细胞几乎消失。兔视网膜下出血在24小时内导致不可逆的视网膜破坏。我们认为,上方视网膜破坏的机制包括血凝块形成的扩散屏障、血凝块收缩对外段的机械损伤以及铁毒性的综合作用。