The purpose of this project is to create a computational model of a choroidal precapillary arteriole network using computational fluid dynamics modeling (CFD, Fluent, ANSYS, Inc.). The CFD analysis will contain a blood flow model coupled with oxygen (O2) and nitric oxide (NO) transport and reactions. Recently, it was believed that an elevated intraocular pressure (IOP) played an important role in glaucoma development, however recent work has shown that glaucoma can also occur with normotensive IOPs. Unfortunately the step-by-step progression of the disease is not well understood and currently the only known modifiable risk factor is the elevated IOP. The increased pressure may be due to excess NO, linking increased vasodilatation directly to the raised IOP. NO generation mostly occurs within the endothelium and is directly related to the local oxygen concentration although there is considerable debate in the literature about the cause of this surplus NO generation. One theory hypothesizes that ischemic regions within the choroid is responsible for the elevated NO levels and another is that reperfusion injuries cause the elevated NO levels. The relationship between these theories, IOP, and retinal ganglion cell (RGC) death (glaucoma), are not well understood. The purpose of this CFD model is to provide a quantitative analysis of blood flow and gas transport within the eye and to look at the plausibility of ischemic regions and reperfusion injuries causing glaucomic neurodegeneration. Concentrations and distributions of O2 and NO will be modeled throughout the arteriole network and surrounding tissue. This work will provide the preliminary quantitative framework needed to investigate the role of excessive NO generation on glaucoma development.

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