title: Effect(s) of preterm birth on normal retinal vascular development and oxygen-induced retinopathy in the neonatal rat.
abstract: OBJECTIVE
  Maturity is a critical factor in the pathogenesis of retinopathy of prematurity (ROP). One widely used method for studying this condition is that of oxygen-induced retinopathy (OIR). The general conditions of an OIR term animal, both at the time of birth and following birth, differ from those of the preterm infant. This, to simulate preterm conditions and to provide a basis for further studies on ROP, we investigated the effect(s) of preterm birth on retinal vascularization using the neonatal rat.
  
  
  METHODS
  Sprague-Dawley (SD) rats were delivered preterm by caesarean section on the day 19 of gestation. Term pups were used as controls. On the day of birth, preterm and term pups were housed under conditions of room air or cyclic oxygen. Retinas of pups housed in room air on days 4, 7, 10, 14, 18 and 22, as well as pups housed in oxygen on days 14, 18, and 22 were whole-mounted and stained with isolectin-B4. On day 18, cross-sections of the retina were cut and stained with hematoxylin and eosin for the identification of preretinal neovascular tufts. Images of avascular and neovascular areas were compared using light and fluorescence microscopy.
  
  
  RESULTS
  Preterm pups had significantly larger avascular retinal areas than term rats on the various postnatal days. After exposure to cyclic oxygen, preterm pups demonstrated significantly larger avascular (days 14 and 18) and neovascular areas (day 18) compared with term rats. On day 22, residual retinopathy of preterm pups was greater than that of term pups.
  
  
  CONCLUSIONS
  Preterm birth of rats, which are comparable in their physiology to humans, had negative effects on retinal vascularization. The impaired retinal vascular development and subsequent vasoproliferation resulting from hyperoxia in preterm pups is more severe and enduring.
authors.affiliation: Department of Ophthalmology, Xijing Hospital, Fourth Military Medical University , Xi'an, Shaanxi , China.
authors.forename: Rong
authors.initials: R
authors.lastname: Li
authors.forename: Xiangmin
authors.initials: X
authors.lastname: Yang
authors.forename: Yusheng
authors.initials: Y
authors.lastname: Wang
authors.forename: Zhaojie
authors.initials: Z
authors.lastname: Chu
authors.forename: Tao
authors.initials: T
authors.lastname: Liu
authors.forename: Tong
authors.initials: T
authors.lastname: Zhu
authors.forename: Xiang
authors.initials: X
authors.lastname: Gao
authors.forename: Zhen
authors.initials: Z
authors.lastname: Ma
mesh_terms: D000388:Air; D000818:Animals; D000831:Animals, Newborn; D001485:Basement Membrane / Q000254:growth & development / Q000473:pathology; D001724:Birth Weight; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000254:growth & development / Q000473:pathology; D005260:Female; D005865:Gestational Age; D018496:Hyperoxia / Q000209:etiology / Q000473:pathology; D008297:Male; D010100:Oxygen / Q000633:toxicity*; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D012160:Retina / Q000254:growth & development* / Q000473:pathology; D015861:Retinal Neovascularization / Q000209:etiology / Q000473:pathology*; D012171:Retinal Vessels / Q000254:growth & development* / Q000473:pathology; D012178:Retinopathy of Prematurity / Q000209:etiology / Q000473:pathology*
chemical_list: D010100:Oxygen