title: Limiting photoreceptor death and deconstruction during experimental retinal detachment: the value of oxygen supplementation.
abstract: OBJECTIVE
  To assess the role of hypoxia in causing the death and deconstruction of photoreceptors in detached retinas and the effectiveness of supplemental oxygen in limiting such damage.
  
  
  METHODS
  Retinal detachment was induced surgically in the right eye of each of 10 cats. The cats were allowed to survive surgery for 3 days. Two were kept for these 3 days in normoxia (room air, 21% oxygen) and eight in hyperoxia (70% oxygen). The retinas were examined for cell death by use of labels for normal and fragmenting DNA, with antibodies and a cone sheath-specific lectin to demonstrate the status of their inner and outer segments, the synaptic structures of the outer plexiform layer, and the distribution of basic fibroblast growth factor (bFGF) and with in situ hybridization to demonstrate bFGF mRNA.
  
  
  RESULTS
  Retinal detachment without oxygen supplementation caused the death of some photoreceptors; the loss of cytochrome oxidase from the inner segments and the collapse of the outer segments of surviving photoreceptors; the loss of synaptophysin profiles from the outer plexiform layer; and the loss of bFGF protein from retinal neurons and neuroglia but not from retinal vessels. Oxygen supplementation (hyperoxia) during detachment mitigated all these changes, reducing photoreceptor death, maintaining the specialized structures of surviving photoreceptors, and stabilizing the bFGF within the retina.
  
  
  CONCLUSIONS
  In experimental retinal detachment, hypoxia caused by the separation of outer retina from its normal source of nutrients is a factor in inducing the death and deconstruction of photoreceptors as well as in the loss of bFGF from the detached retina. Hyperoxia offered to human patients between diagnosis of retinal detachment and surgery may enhance the function of the reattached retina.
authors.affiliation: New South Wales Retinal Dystrophy Research Centre, Department of Anatomy and Histology, University of Sydney, Australia.
authors.forename: K
authors.initials: K
authors.lastname: Mervin
authors.forename: K
authors.initials: K
authors.lastname: Valter
authors.forename: J
authors.initials: J
authors.lastname: Maslim
authors.forename: G
authors.initials: G
authors.lastname: Lewis
authors.forename: S
authors.initials: S
authors.lastname: Fisher
authors.forename: J
authors.initials: J
authors.lastname: Stone
mesh_terms: D000818:Animals; D017209:Apoptosis; D002415:Cats; D002470:Cell Survival; D004247:DNA / Q000032:analysis; D053938:DNA Fragmentation; D004195:Disease Models, Animal; D003576:Electron Transport Complex IV / Q000378:metabolism; D016222:Fibroblast Growth Factor 2 / Q000235:genetics / Q000378:metabolism; D000860:Hypoxia / Q000209:etiology* / Q000473:pathology; D017403:In Situ Hybridization; D010102:Oxygen Inhalation Therapy; D020419:Photoreceptor Cells, Vertebrate / Q000378:metabolism / Q000473:pathology*; D012333:RNA, Messenger / Q000378:metabolism; D012163:Retinal Detachment / Q000150:complications* / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D016708:Synaptophysin / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D012333:RNA, Messenger; D016708:Synaptophysin; D016222:Fibroblast Growth Factor 2; D004247:DNA; D003576:Electron Transport Complex IV