“…[10][11][12][13][14][15][16][17][18] The authors of multiple reports [19][20][21][22][23][24][25] have demonstrated a marked increase in both the incidence and severity of ROP in humans and related neovascular retinopathies in other mammals after oxygen supplementation. Aggressive supplemental oxygenation of premature infants also strains the health care system both in the extended duration of therapy as well as more intensive outpatient care not necessary for infants with a more moderate oxygen saturation target.…”
Section: Discussionmentioning
confidence: 99%
“…Aggressive supplemental oxygenation of premature infants also strains the health care system both in the extended duration of therapy as well as more intensive outpatient care not necessary for infants with a more moderate oxygen saturation target. 10,26 However, although lower levels of oxygen supplementation do result in a lower incidence of ROP and related neovascular retinopathies in other mammals, [10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25] overaggressive limitation of oxygen to less physiologic levels may increase morbidity and mortality, 18,27,28 although a more physiologic reduction could be less detrimental. 29 In this study we compared the incidence and severity of ROP during the 2 years immediately before and the 2 years immediately after the initiation of a new oxygen protocol targeting oxygen saturations at 85% to 93% for all inborn premature infants at a level III neonatal intensive care unit (NICU).…”
“…[10][11][12][13][14][15][16][17][18] The authors of multiple reports [19][20][21][22][23][24][25] have demonstrated a marked increase in both the incidence and severity of ROP in humans and related neovascular retinopathies in other mammals after oxygen supplementation. Aggressive supplemental oxygenation of premature infants also strains the health care system both in the extended duration of therapy as well as more intensive outpatient care not necessary for infants with a more moderate oxygen saturation target.…”
Section: Discussionmentioning
confidence: 99%
“…Aggressive supplemental oxygenation of premature infants also strains the health care system both in the extended duration of therapy as well as more intensive outpatient care not necessary for infants with a more moderate oxygen saturation target. 10,26 However, although lower levels of oxygen supplementation do result in a lower incidence of ROP and related neovascular retinopathies in other mammals, [10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25] overaggressive limitation of oxygen to less physiologic levels may increase morbidity and mortality, 18,27,28 although a more physiologic reduction could be less detrimental. 29 In this study we compared the incidence and severity of ROP during the 2 years immediately before and the 2 years immediately after the initiation of a new oxygen protocol targeting oxygen saturations at 85% to 93% for all inborn premature infants at a level III neonatal intensive care unit (NICU).…”
“…During the 1950's, results gained from the mouse model of oxygen-induced retinopathy [2,3] corroborated findings of the kitten model where it was shown that exposure of newborn kittens to high ambient oxygen could subsequently lead to the production of a proliferative retinopathy [4]. Since then, there has been little new work on the mouse model as an animal model of the proliferative phase of retinopathy of prematurity (ROP) in particular and of the proliferative retinopathies in general.…”
Newborn mice exposed to high (greater than 98%) ambient oxygen during the newborn period and subsequently removed to room air will develop a proliferative retinopathy which mimics the neovascular component of acute retinopathy of prematurity. In this paper, we report preliminary ultrastructural findings on the vitreous new vessels in the mouse model of oxygen-induced retinopathy, and argue that the model is appropriate for research on non surgical treatments for ROP in particular and angiogenesis in general.
“…Several workers produced or evaluated evidence pertaining to the rate of oxygen administration in the etiology of retrolental fibroplasia (1,14,15,16,17,80,89,93,113,118,122,123,124,125,155,162,177,179,187,189,219,252,259,260,342).…”
Section: Retrolental Fibroplasia (Retinopathy Of Prematurity)mentioning
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