title: The efficacy of delayed oxygen therapy in the treatment of experimental retinal detachment.
abstract: OBJECTIVE
  To evaluate the ability of delayed hyperoxia to slow or prevent degenerative and gliotic changes initiated by retinal detachment.
  
  
  METHODS
  An experimental study.
  
  
  METHODS
  Rhegmatogenous detachments were produced in the right eyes of eight cats. After 1 day in room air (21% O(2)), four cats were placed in chambers with the O(2) concentration regulated at 70%; the other four were left in room air. At 7 days the retinas were harvested and examined by light and confocal microscopy. Cell specific antibodies, TUNEL and proliferation assays, outer segment length, and photoreceptor counts, were used to assess the condition of the retina. The contralateral unoperated eyes were used as controls.
  
  
  RESULTS
  Animals maintained in elevated O(2) showed a dramatic preservation of rod and cone outer segments as well as in the organization of the outer plexiform layer. The number of surviving photoreceptors was increased in the hyperoxia-treated animals. Neurite sprouting, a characteristic of detached retina, was rarely observed in the experimental eyes. Proliferation of non-neuronal cells was reduced, but not halted, by hyperoxia. GFAP and vimentin expression was not effected by hyperoxia; these intermediate filament proteins increased in Müller cells similar to that observed in control detachments.
  
  
  CONCLUSIONS
  Exposure to hyperoxia, delayed by 1 day after the onset of retinal detachment, was highly effective in preserving photoreceptor cells and in reducing proliferation within the retina. It did not, however, reduce the hypertrophy of Müller glia. There were no apparent detrimental effects of exposure to 70% O(2) for 6 days. These results suggest that human patients may benefit from breathing elevated oxygen levels while awaiting reattachment surgery, even if the hyperoxia is delayed relative to the time of detachment.
authors.affiliation: Neuroscience Research Institute, University of California, Santa Barbara, 93106, USA. g_lewis@lifesci.ucsb.edu
authors.forename: Geoffrey P
authors.initials: GP
authors.lastname: Lewis
authors.forename: Kevin C
authors.initials: KC
authors.lastname: Talaga
authors.forename: Kenneth A
authors.initials: KA
authors.lastname: Linberg
authors.forename: Robert L
authors.initials: RL
authors.lastname: Avery
authors.forename: Steven K
authors.initials: SK
authors.lastname: Fisher
mesh_terms: D000818:Animals; D002415:Cats; D002452:Cell Count; D002455:Cell Division; D002470:Cell Survival; D004195:Disease Models, Animal; D005136:Eye Proteins / Q000378:metabolism; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D018496:Hyperoxia / Q000503:physiopathology; D006984:Hypertrophy; D020287:In Situ Nick-End Labeling; D018613:Microscopy, Confocal; D009457:Neuroglia / Q000473:pathology; D010102:Oxygen Inhalation Therapy; D020419:Photoreceptor Cells, Vertebrate / Q000378:metabolism / Q000473:pathology; D012163:Retinal Detachment / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D013997:Time Factors; D014746:Vimentin / Q000378:metabolism
chemical_list: D005136:Eye Proteins; D005904:Glial Fibrillary Acidic Protein; D014746:Vimentin