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Fetal growth restriction induced by chronic placental insufficiency has long-term effects on the retina but not the optic nerve.
- Source :
-
Investigative ophthalmology & visual science [Invest Ophthalmol Vis Sci] 2005 Sep; Vol. 46 (9), pp. 3300-8. - Publication Year :
- 2005
-
Abstract
- Purpose: Reduced birth weight is associated with an increased risk of visual impairments. This study was undertaken to determine whether prenatal exposure to a chronic compromise sufficient to cause fetal growth restriction (FGR) results in long-term alterations to the retina and optic nerve.<br />Methods: FGR was induced by umbilicoplacental embolization (UPE) in two cohorts of pregnant ewes from (1) 120 days of gestation (dg) until 140 dg and (2) 120 dg until term ( approximately 147 dg). Control fetuses were not subjected to UPE. The structure and neurochemistry of the retina and number and structure of ganglion cell axons were assessed in near-term (140 dg) and adult animals (2.3 years).<br />Results: In near-term FGR fetuses compared with control fetuses there were significant reductions (P < 0.05) in the outer plexiform layer (OPL), the photoreceptor inner and outer segment layers, the inner nuclear layer (INL) in the central retina and the outer nuclear layer (ONL) in the peripheral retina, and the diameter of ganglion cell axons in the optic nerve, with a proportional reduction in the thickness of myelin sheaths. In FGR animals compared with the control at 2.3 years, there were significant reductions (P < 0.05) in the total thickness of the retina, the thickness of the photoreceptor outer segment layer and the INL and the number of tyrosine hydroxylase-immunoreactive (TH-IR) dopaminergic amacrine cells. Axonal diameter and myelin sheath thickness in the optic nerve were not different (P > 0.05) between groups.<br />Conclusions: Chronic placental insufficiency in late gestation results in long-lasting effects on specific retinal components, including photoreceptor outer segments and TH-IR amacrine cells. Other alterations observed at term, including reductions in growth and myelination of optic nerve axons, do not persist, suggesting delayed rather than permanently compromised development. Alterations persisting into adulthood could affect visual function.
- Subjects :
- Amacrine Cells pathology
Animals
Axons pathology
Cell Count
Cell Survival
Chronic Disease
Disease Models, Animal
Female
Fetal Growth Retardation physiopathology
Immunohistochemistry
Optic Nerve pathology
Optic Nerve Diseases physiopathology
Organ Size
Photoreceptor Cells, Vertebrate pathology
Pregnancy
Retina pathology
Retinal Diseases physiopathology
Retinal Ganglion Cells pathology
Sheep
Fetal Growth Retardation etiology
Optic Nerve embryology
Optic Nerve Diseases etiology
Placental Insufficiency complications
Retina embryology
Retinal Diseases etiology
Subjects
Details
- Language :
- English
- ISSN :
- 0146-0404
- Volume :
- 46
- Issue :
- 9
- Database :
- MEDLINE
- Journal :
- Investigative ophthalmology & visual science
- Publication Type :
- Academic Journal
- Accession number :
- 16123433
- Full Text :
- https://doi.org/10.1167/iovs.04-1357