Analysis of animal models of macular edema

• Published in: Survey of ophthalmology Vol. 28; pp. 520 - 524
• Main Author: Bellhorn, Roy W.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.05.1984
• Subjects: animal models; Animals; blood-ocular barriers; Capillary Permeability; Cataract Extraction - adverse effects; Ciliary Body - surgery; Cryosurgery - adverse effects; cystoid macular edema; Edema - etiology; Fovea Centralis - injuries; Infarction - complications; Infarction - etiology; Lasers - adverse effects; Light - adverse effects; Macaca mulatta; macular edema; Macular Edema - etiology; Macular Edema - physiopathology; retinal anatomy; Retinal Diseases - etiology; retinal edema; Retinal Vessels - physiopathology; subhuman primates; Talc - adverse effects; retinal anatomy; animal models; blood-ocular barriers; retinal edema; macular edema; subhuman primates; cystoid macular edema
• ISSN: 0039-6257; 1879-3304
• 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 macular 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.