Limiting the proliferation and reactivity of retinal muller cells during experimental retinal detachment: The value of oxygen supplementation

PURPOSE: To assess the role of hypoxia in inducing the proliferation, hyper trophy, and dysfunction of Muller cells in detached retina and the effectiv eness of supplemental oxygen in limiting these reactions. METHODS: Retinal detachments were produced in the right eye of each of 13 c ats; the cats survived surgery for 3 days, during which six were kept in no rmoxia (room air, 21%) and seven in hyperoxia (70% oxygen). Retinas were la beled for proliferation with an antibody (MIB-1) to a cell cycle protein (K i-67), for evidence of hypertrophy employing antibodies to the intermediate filament protein glial fibrillary acidic protein (GFAP) and to p-tubulin a nd for disturbance of glutamate neurochemistry employing antibodies to glut amate to a glutamate receptor (GluR-2) and to glutamine synthetase. RESULTS: Results from the two animals kept in normoxia after retinal detach ment confirmed previous reports that detachment caused the proliferation of Muller cells, the hypertrophy of Muller cell processes, and the disruption of glutamate recycling by Muller cells. Oxygen supplementation during deta chment reduced Muller cell proliferation and hypertrophy and reduced the ab normalities in the distributions of glutamate, GluR-2, and glutamine synthe tase. CONCLUSIONS: Oxygen supplementation reduced the reaction of retinal Muller cells to retinal detachment, limiting their proliferation and helping to ma intain their normal structure and function. In the clinical setting, oxygen supplementation between diagnosis and reattachment surgery may reduce the incidence and severity of glial-based complications, such as proliferative vitreoretinopathy. (C) 1999 by Elsevier Science Inc. All rights reserved.