Lukas Holsen

Abstract

The purpose of this project is to create a computational model of a precapillary arteriole network near the optic nerve head (ONH) 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. Until recently it was believed that elevated intraocular pressure (IOP) was causal in glaucoma, however recent studies demonstrate that glaucoma is associated with sensitivity to IOP itself. Because of this insight, other mechanisms besides mechanical damage that could cause glaucomatous neurodegeneration need to be explored, such as alterations in blood flow and oxygenation due to systemic changes. Excessive NO has often been associated with glaucoma and can cause increased vasodilation. NO has also been shown to have neurotoxic effects on the ONH when available in excess. 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 surplus NO generation. Several theories exist attempting to explain this surplus production. One theory proposes that surplus NO is generated in ischemic regions within the choroid, the vascular layer of tissue that provides nutrient transport to different layers of the eye. Others suggest that the NO is produced due to reperfusion injuries and a third proposes the failure of autoregulation may cause the surplus NO. 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 framework for the analysis of blood flow and gas transport within the eye and to look at the contribution of ischemic regions, reperfusion injuries, and/or the failure of autoregulation leading to glaucomatous neurodegeneration. Concentrations and distributions of O2 and NO will be modeled throughout an arteriole network and surrounding tissue to predict what concentration is ultimately delivered to the ONH. This work will provide the preliminary quantitative framework that is needed to determine the role of excessive NO generation on glaucoma development and provide a framework for further species transport modeling in the eye.

Library of Congress Subject Headings

Oxygen--Physiological transport--Mathematical models; Nitric oxide--Physiological transport--Mathematical models; Glaucoma--Prevention--Research

Publication Date

11-3-2011

Document Type

Thesis

Department, Program, or Center

Mechanical Engineering (KGCOE)

Advisor

Lamkin-Kennard, Kathleen

Comments

Note: imported from RIT’s Digital Media Library running on DSpace to RIT Scholar Works. Physical copy available through RIT's The Wallace Library at: TA357 .H65 2011

Campus

RIT – Main Campus

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