Abstract
Impaired blood flow and oxygenation contribute to many ocular pathologies, including glaucoma. Here, a mathematical model is presented that combines an image-based heterogeneous representation of retinal arterioles with a compartmental description of capillaries and venules. The arteriolar model of the human retina is extrapolated from a previous mouse model based on confocal microscopy images. Every terminal arteriole is connected in series to compartments for capillaries and venules, yielding a hybrid model for predicting blood flow and oxygenation throughout the retinal microcirculation. A metabolic wall signal is calculated in each vessel according to blood and tissue oxygen levels. As expected, a higher average metabolic signal is generated in pathways with a lower average oxygen level. The model also predicts a wide range of metabolic signals dependent on oxygen levels and specific network location. For example, for high oxygen demand, a threefold range in metabolic signal is predicted despite nearly identical PO2 levels. This whole-network approach, including a spatially nonuniform structure, is needed to describe the metabolic status of the retina. This model provides the geometric and hemodynamic framework necessary to predict ocular blood flow regulation and will ultimately facilitate early detection and treatment of ischemic and metabolic disorders of the eye.
Highlights
Eye disease and associated blindness are highly impactful to both individuals and society as a whole
The current study demonstrated the interconnection of all vessels in an arteriolar network such that the metabolic signal in a given vessel is dependent upon all other vessels in the network
The ability to predict changes in arteriolar diameter and blood flow in a heterogeneous retinal microvascular network in response to changes in blood pressure or oxygen demand is critical for unraveling mechanisms involved in many ocular pathologies, especially open-angle glaucoma (OAG)
Summary
Eye disease and associated blindness are highly impactful to both individuals and society as a whole. A unified theory of the structural and hemodynamic factors that combine to cause functional visual impairment in glaucoma is missing. Other diseases such as diabetic retinopathy have clear vascular involvement and clinical presentation but lack a robust understanding of prior sequential events and/or individual susceptibility. In both examples, there are significant gaps in knowledge related to the retinal microvasculature, tissue oxygenation, and retinal regulatory capacity during stresses related to disease processes
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