Bellhorn R W
Surv Ophthalmol. 1984 May;28 Suppl:520-4. doi: 10.1016/0039-6257(84)90235-2.
Various models of macular edema have been studied; however, frank development of a prototypical cystoid macular edema has not been observed. In humans, cystoid edema is frequently observed in association with other disturbances of the retina. Thus, a basic drawback of the animal models may be that an otherwise healthy retina is capable of resolving the experimentally produced edema, thereby preventing chronic cystoid maculopathy. A review of macular edema models and of experimental retinal and brain edema investigations suggests that blood-retinal (blood-brain) barrier permeability abnormalities need to be accompanied by ineffective edema resolving mechanisms for the production of a chronic edema. Intraglial uptake of extravasated serum proteins has been hypothesized to be an edema-resolving mechanism in brain edema. As such, the hypothesis that the Müller cell may be important to edema resolution appears attractive. Future animal model studies should include methodologies whereby edema resolution mechanisms are impaired.
已经对各种黄斑水肿模型进行了研究；然而，尚未观察到典型的囊样黄斑水肿的明显发展。在人类中，囊样水肿经常与视网膜的其他病变相关联。因此，动物模型的一个基本缺点可能是，原本健康的视网膜能够消退实验性产生的水肿，从而预防慢性囊样黄斑病变。对黄斑水肿模型以及实验性视网膜和脑水肿研究的综述表明，血视网膜（血脑）屏障通透性异常需要伴有无效的水肿消退机制才能产生慢性水肿。神经胶质细胞对渗出的血清蛋白的摄取被认为是脑水肿的一种水肿消退机制。因此， Müller细胞可能对水肿消退很重要这一假设似乎很有吸引力。未来的动物模型研究应包括损害水肿消退机制的方法。
