title: Retinal thickness and subnormal retinal oxygenation response in experimental diabetic retinopathy.
abstract: OBJECTIVE
  To test the hypothesis that subnormal retinal oxygenation response (DeltaPo2) found at 3 months of experimental diabetes is associated with cellular swelling and increased retinal thickness.
  
  
  METHODS
  Two groups of animals were studied: control rats injected intraperitoneally with either 15% body weight of saline or distilled water (cellular swelling model) or with intravitreal N-methyl-D-aspartate (NMDA) and 3-month-old diabetic and age-matched control rats. Intraocular pressure and retinal thickness was assessed using an applanation tonometer or high-resolution MRI (23.4 microm2 in-plane). In separate studies, functional MRI was used to measure blood-retinal barrier (BRB) integrity after Gd-DTPA injection intravenously and retinal DeltaPo2 during carbogen provocation.
  
  
  RESULTS
  Inner and total retinal thickness were lower (P < 0.05) after NMDA injection, not different (P > 0.05) between control, before and after saline injection and before distilled water injection, and supernormal (P < 0.05) after distilled water injection. In diabetic rats, thickness was normal (P > 0.05) at most distances from the optic nerve but was subnormal (P < 0.05) in superior retina (0.5 mm from the optic nerve). Intraocular pressure was not different (P > 0.05) between groups. BRB was intact (P > 0.05) after saline and distilled water injection. DeltaPo2 was normal (P > 0.05) after saline injection and over inferior hemiretina of the diabetic group but was subnormal (P < 0.05) after distilled water injection and over superior hemiretina of diabetic rats.
  
  
  CONCLUSIONS
  The lack of increased thickness in 3-month-old diabetic rats in vivo raises the possibility that intracellular swelling is unlikely to underlie subnormal DeltaPo2 in experimental diabetes. In diabetic rats, the spatial disconnect between subnormal DeltaPo2 pansuperiorly and retinal thinning only superiorly to the optic nerve suggests that neurovascular coupling is perturbed.
authors.affiliation: Department of Anatomy and Cell Biology, Wayne State University, Detroit, MI 48201, USA.
authors.forename: Hongmei
authors.initials: H
authors.lastname: Luan
authors.forename: Robin
authors.initials: R
authors.lastname: Roberts
authors.forename: Matthew
authors.initials: M
authors.lastname: Sniegowski
authors.forename: Dennis J
authors.initials: DJ
authors.lastname: Goebel
authors.forename: Bruce A
authors.initials: BA
authors.lastname: Berkowitz
mesh_terms: D000818:Animals; D001813:Blood-Retinal Barrier; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000473:pathology; D003930:Diabetic Retinopathy / Q000378:metabolism / Q000473:pathology*; D018690:Excitatory Amino Acid Agonists / Q000008:administration & dosage; D007429:Intraocular Pressure; D008269:Macular Edema / Q000139:chemically induced / Q000473:pathology; D008279:Magnetic Resonance Imaging; D016202:N-Methylaspartate / Q000008:administration & dosage; D010100:Oxygen / Q000378:metabolism; D010101:Oxygen Consumption; D010313:Partial Pressure; D051381:Rats; D017207:Rats, Sprague-Dawley; D012160:Retina / Q000187:drug effects / Q000473:pathology*; D014065:Tonometry, Ocular; D014867:Water / Q000008:administration & dosage
chemical_list: D018690:Excitatory Amino Acid Agonists; D014867:Water; D016202:N-Methylaspartate; D010100:Oxygen