BACKGROUND: Using laser speckle flowgraphy to calculate retinal blood flow, we sought to measure changes in optic nerve blood flow compared to the normal fellow eye (relative blood flow) and changes in vision in patients with central retinal artery occlusions of varying duration. METHODS: Laser speckle flowgraphy was used to measure optic nerve blood flow in eyes with central retinal artery occlusions and the normal fellow eye of patients seen at Beth Israel Deaconess Medical Center to calculate relative blood flow. Visual acuity was assessed monocularly using Snellen Charts in a standardized fashion. RESULTS: In healthy control patients (n=20), relative blood flow was calculated to be 1.02 (p= 0.6843), indicating no significant difference in blood flow between eyes. In patients with unilateral central retinal artery occlusions (n=7), relative blood flow was calculated to be 0.66 ± 0.13 (p < .001), indicating on average a 33 percent loss in blood flow through the optic nerve head. When comparing relative blood flow values of CRAO patients measured within one year of vision loss versus patients when measured after one year of reported vision loss, values of patients measured within one year were lower. CONCLUSIONS AND RELEVANCE: Laser Speckle Flowgraphy has been shown to be a useful diagnostic tool that can reliably provide quantitative information on retinal blood flow. Results suggest that blood flow through the optic nerve head does return over time, presumably as the occlusion resolves or recanalizes. Longitudinal analysis determined a higher relative blood flow in patients one-year post incident versus within one year. However no statistically significant difference in visual acuity between these groups was found, indicating that return of blood flow is not associated with a return in visual acuity. Relative blood flow may be a useful measure of retinal perfusion in other retinal vascular disorders.

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Master of Science / Department of Kinesiology / Brett J. Wong / Mechanisms underlying the cutaneous vasodilation response to local skin heating and whole body heating in humans remain unresolved. Although nitric oxide (NO) is known to contribute to these responses, it remains unclear as to the source of NO. Adenosine receptors induce vasodilation in many human tissues and may work, in part, through NO. As these receptors are also known to be located in the cutaneous vasculature, the studies contained in this thesis were designed to investigate a potential contribution of adenosine receptor activation to the rise in skin blood flow elicited by local skin and whole body heating. The study presented in chapter IV was designed to determine a potential role for adenosine receptors in contributing to cutaneous thermal hyperemia. Four cutaneous microdialysis sites were randomly assigned one of four drug treatments designed to elucidate the contribution of A[subscript]1/A[subscript]2 adenosine receptors during local skin heating. Each site was locally heated from a baseline temperature of 33°C to 42°C at a rate of 1°C/10 s and skin blood flow was monitored via laser-Doppler flowmetry (LDF). The data obtained from these experiments suggest A[subscript]1/A[subscript]2 adenosine receptor activation directly contributes to cutaneous thermal hyperemia. These data further suggest a portion of the NO response may be explained by A[subscript]1/A[subscript]2 adenosine receptor activation; however, a substantial portion of the NO response is independent of the adenosine receptor contribution. The study presented in chapter V was designed to determine a potential role for A[subscript]1/A[subscript]2 adenosine receptors in contributing to cutaneous active vasodilation. Four cutaneous microdialysis sites were randomly assigned one of four drug treatments, as above, and skin blood flow was monitored via LDF. Whole body heat stress, sufficient to raise oral temperature at least 0.8°C above baseline, was induced via water-perfused suits. The data obtained from these experiments suggest A[subscript]1/A[subscript]2 adenosine receptor activation does not directly contribute to cutaneous active vasodilation; however, a role for A[subscript]1/A[subscript]2 adenosine receptor activation is unmasked when NO synthase is inhibited. The data from this study further suggest that A[subscript]1/A[subscript]2 adenosine receptor activation may be responsible for a portion of the known NO component of cutaneous active vasodilation.

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