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Christina Seide, Marina Garcia Garrido, Vithiyanjali Sothilingam, Naoyuki Tanimoto, Susanne Beck, Mathias Seeliger; Persistent hyaloid vessels counteract insufficient retinal perfusion in the mouse eye. Invest. Ophthalmol. Vis. Sci. 2013;54(15):4639.
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Persistence of embryonic vitreal vasculature beyond the time of its physiologic regression during ocular development was observed in a number of mouse models where retinal vascularization is impaired. Here, we evaluate the nature and distribution of persistent hyaloid vessels in relation to the topography of retinal perfusion defects
In vivo imaging was performed with a Heidelberg Engineering HRA I using native confocal scanning-laser ophthalmoscopy (cSLO) as well as fluorescein (FA) and indocyanine green angiography (ICGA). Mouse models with insufficiencies in retinal vascularization already starting during development were selected for this study. The setting of different confocal planes allowed a selective analysis of the distribution of hyaloid and retinal surface vasculature. The topography of vascular alterations of retinal vessels was then correlated with the distribution of vitreal vascular persistence.
The combination of FA and ICGA revealed a detailed overview of the distribution of retinal vessels and their state of perfusion. Retinal regions with a reduced or lacking circulation could often be identified via a leakage of fluorescein indicating enhanced vascular ultrafiltration due to VEGF upregulation in dependent tissues. In all cases studied, areas of insufficient retinal perfusion colocalized with persistent hyaloid vasculature. The strongest inhibition of hyaloid vessel regression was present in mice with a total lack of parts of the retinal vasculature.
The physiology of the regression of vitreal vessels during development is not entirely understood. Some aspects suggest a more or less fixed time window for this process, in particular with respect to the apoptotic death of vascular cells and their removal from the vitreous. On the other hand, we show here that insufficient retinal perfusion, presumably via factors like VEGF, clearly leads to a local persistence of hyaloid vasculature, which in turn improves the compromised perfusion at least for some time. This finding may help to develop symptomatic therapeutic concepts in respective diseases like ROP.
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