Evidence for a critical role of panretinal pathophysiology in experimental ROP.
In this review, we summarize our in vivo studies of retinal pathophysiology in experimental models of retinopathy of prematurity, which were largely focused on the temporal and spatial links between retinal neovascularization (NV), vascular oxygenation, and intraretinal ion regulation. These studies were made possible through the use of magnetic resonance methods. Prior to the phenotype change from normal vessel development to NV, we found little support for a pathogenic role of focal retinal hypoxia at the border of vascular and avascular retina. However, key links were found between retinal NV and functional panretinal defects in both oxygenation to a provocation and intraretinal ion regulation. Through a treatment which reduced NV incidence but not panretinal pathophysiology, proliferative disease was found to last longer than that in the untreated group. These considerations provide compelling evidence that clinical attention directed toward reducing retinal NV should include approaches that reduce functional panretinal pathophysiology.[1]References
- Evidence for a critical role of panretinal pathophysiology in experimental ROP. Berkowitz, B.A., Roberts, R. Doc. Ophthalmol (2010) [Pubmed]
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