title: Alterations of the tunica vasculosa lentis in the rat model of retinopathy of prematurity.
abstract: OBJECTIVE
  To study the relationship between retinal and tunica vasculosa lentis (TVL) disease in retinopathy of prematurity (ROP). Although the clinical hallmark of ROP is abnormal retinal blood vessels, the vessels of the anterior segment, including the TVL, are also altered.
  
  
  METHODS
  ROP was induced in Long-Evans pigmented and Sprague Dawley albino rats; room-air-reared (RAR) rats served as controls. Then, fluorescein angiographic images of the TVL and retinal vessels were serially obtained with a scanning laser ophthalmoscope near the height of retinal vascular disease, ~20 days of age, and again at 30 and 64 days of age. Additionally, electroretinograms (ERGs) were obtained prior to the first imaging session. The TVL images were analyzed for percent coverage of the posterior lens. The tortuosity of the retinal arterioles was determined using Retinal Image multiScale Analysis (Gelman et al. in Invest Ophthalmol Vis Sci 46:4734-4738, 2005).
  
  
  RESULTS
  In the youngest ROP rats, the TVL was dense, while in RAR rats, it was relatively sparse. By 30 days, the TVL in RAR rats had almost fully regressed, while in ROP rats, it was still pronounced. By the final test age, the TVL had completely regressed in both ROP and RAR rats. In parallel, the tortuous retinal arterioles in ROP rats resolved with increasing age. ERG components indicating postreceptoral dysfunction, the b-wave, and oscillatory potentials were attenuated in ROP rats.
  
  
  CONCLUSIONS
  These findings underscore the retinal vascular abnormalities and, for the first time, show abnormal anterior segment vasculature in the rat model of ROP. There is delayed regression of the TVL in the rat model of ROP. This demonstrates that ROP is a disease of the whole eye.
authors.affiliation: Department of Ophthalmology, Boston Children's Hospital, 300 Longwood Avenue, Fegan 4, Boston, MA, 02115, USA.
authors.forename: Tara L
authors.initials: TL
authors.lastname: Favazza
authors.forename: Naoyuki
authors.initials: N
authors.lastname: Tanimoto
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Munro
authors.forename: Susanne C
authors.initials: SC
authors.lastname: Beck
authors.forename: Marina
authors.initials: M
authors.lastname: Garcia Garrido
authors.forename: Christina
authors.initials: C
authors.lastname: Seide
authors.forename: Vithiyanjali
authors.initials: V
authors.lastname: Sothilingam
authors.forename: Ronald M
authors.initials: RM
authors.lastname: Hansen
authors.forename: Anne B
authors.initials: AB
authors.lastname: Fulton
authors.forename: Mathias W
authors.initials: MW
authors.lastname: Seeliger
authors.forename: James D
authors.initials: JD
authors.lastname: Akula
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001160:Arterioles / Q000473:pathology; D004195:Disease Models, Animal; D004596:Electroretinography; D005451:Fluorescein Angiography; D006801:Humans; D007231:Infant, Newborn; D007908:Lens, Crystalline / Q000098:blood supply*; D008297:Male; D010100:Oxygen / Q000633:toxicity; D054514:Persistent Hyperplastic Primary Vitreous / Q000175:diagnosis / Q000503:physiopathology*; D051381:Rats; D020318:Rats, Long-Evans; D017207:Rats, Sprague-Dawley; D012160:Retina / Q000503:physiopathology*; D012161:Retinal Artery / Q000473:pathology*; D015861:Retinal Neovascularization / Q000473:pathology*; D012178:Retinopathy of Prematurity / Q000175:diagnosis / Q000503:physiopathology*
chemical_list: D010100:Oxygen