Fibroblastic Overgrowth of Persistent Tunica Vasculosa Lentis in Premature Infants

Terry, T. L.

doi:10.1001/archopht.1943.00880130074004

Cited by 38 publications

(8 citation statements)

References 7 publications

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“…ROP was first described in 1942 (then termed RLF) as fibroblastic overgrowth of persistent vascular sheath behind each crystalline lens in extreme prematurity [18,19]. RLF was developed in preterm infants in 1949 [20].…”

Section: Discussionmentioning

confidence: 99%

Retinal Protective Effects of Resveratrol via Modulation of Nitric Oxide Synthase on Oxygen-induced Retinopathy

Kim

Suh

2010

Korean J Ophthalmol

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PurposeRetinopathy of prematurity (ROP) is one of the leading causes of blindness, with retinal detachment occurring due to oxygen toxicity in preterm infants. Recently, advances in neonatal care have led to improved survival rates for preterm infants, and ROP has increased in incidence. In the present study, we aimed to determine whether or not resveratrol exhibits protective effects in an animal model of ROP and in primary retinal cell cultures of neonatal rat via nitric oxide (NO)-modulating actions using western blotting and real-time PCR with inducible nitric oxide synthase (iNOS), endothelial NOS (eNOS) and neuronal NOS (nNOS) antibodies and mRNAs.MethodsIn an in vivo oxygen-induced retinopathy (OIR) model, cyclic hyperoxia was induced with 80% O2 for one day and 21% O2 for one day from P1 to P14 in newborn Sprague-Dawley (SD) rats. Resveratrol was injected intravitreally for seven days and rats were sacrificed at P21. In vitro OIR primary retinal cell culture was performed using P0-2 SD rats. Hyperoxia injuries were induced through 100% O2 exposure for six hours. Western blotting and real-time PCR using iNOS, eNOS, nNOS antibodies and primers were performed in the rat model of ROP and the dispersed retinal cell culture.ResultsIn both in vivo and in vitro OIR, the expression of iNOS antibody and mRNA was increased and of eNOS and nNOS were reduced in the resveratrol-treated group.ConclusionsIn conclusion, resveratrol appeared to exert retinal protective effects via modulation of NO-mediated mechanism in in vivo and in vitro OIR models.

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Section: Discussionmentioning

confidence: 99%

Retinal Protective Effects of Resveratrol via Modulation of Nitric Oxide Synthase on Oxygen-induced Retinopathy

Kim

Suh

2010

Korean J Ophthalmol

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“…The first case of ROP was described in Boston by Dr TL Terry in 1942 [2]. However, he did recognize the salient epidemiology and showed that the disease occurred much more frequently in infants born extremely prematurely [3]. In a second report [3], containing several pathological specimens in the cicatricial end stages of the disease with multiples complications, Terry clearly misinterpreted the involved pathophysiology.…”

Section: Historical Backgroundmentioning

confidence: 99%

“…The condition was previously called retrolental fibroplasia (RLF), because the scar is white and visible through the pupil [3]. Stage 5 in its most severe form shows a dense white membrane or scar behind the lens of the eye.…”

Section: Stages In Ropmentioning

confidence: 99%

Retinopathy of Prematurity

Rivera¹,

Duchemin-Kermorvant²,

Dorfman³

et al. 2012

Neonatology

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“…Retinopathy of prematurity (ROP), once known as retrolental fibroplasia, is an ocular disease associated with premature babies. Terry [21] first described ROP in 1943. Currently, the incidence of ROP is about 10% for newborns with low birth weight [22, 23].…”

Section: Retinopathy Of Prematuritymentioning

confidence: 99%

Protective effects of melatonin in experimental free radical‐related ocular diseases

Siu

Maldonado

Sánchéz-Hidalgo

et al. 2006

Journal of Pineal Research

151

118

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: Melatonin (N‐acetyl‐5‐methoxytryptamine) is an indoleamine with a range of antioxidative properties. Melatonin is endogenously produced in the eye and in other organs. Current evidence suggests that melatonin may act as a protective agent in ocular conditions such as photo‐keratitis, cataract, glaucoma, retinopathy of prematurity and ischemia/reperfusion injury. These diseases are sight‐threatening and they currently remain, for the most part, untreatable. The pathogenesis of these conditions is not entirely clear but oxidative stress has been proposed as one of the causative factors. Elevated levels of various reactive oxygen and nitrogen species have been identified in diseased ocular structures. These reactants damage the structure and deplete the eye of natural defense systems, such as the antioxidant, reduced glutathione, and the antioxidant enzyme superoxide dismutase. Oxidative damage in the eye leads to apoptotic degeneration of retinal neurons and fluid accumulation. Retinal degeneration decreases visual sensitivity and even a small change in the fluid content of the cornea and crystalline lens is sufficient to disrupt ocular transparency. In the eye, melatonin is produced in the retina and in the ciliary body. Continuous regeneration of melatonin in the eye offers a frontier antioxidative defense for both the anterior and posterior eye. However, melatonin production is minimal in newborns and its production gradually wanes in aging individuals as indicated by the large drop in circulating blood concentrations of the indoleamine. These individuals are possibly at risk of contracting degenerative eye diseases that are free radical‐based. Supplementation with melatonin, a potent antioxidant, in especially the aged population should be considered as a prophylaxis to preserve visual functions. It may benefit many individuals worldwide, especially in countries where access to medical facilities is limited.

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Fibroblastic Overgrowth of Persistent Tunica Vasculosa Lentis in Premature Infants

Cited by 38 publications

References 7 publications

Retinal Protective Effects of Resveratrol via Modulation of Nitric Oxide Synthase on Oxygen-induced Retinopathy

Retinal Protective Effects of Resveratrol via Modulation of Nitric Oxide Synthase on Oxygen-induced Retinopathy

Retinopathy of Prematurity

Protective effects of melatonin in experimental free radical‐related ocular diseases

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