Diabetic retinopathy (DR) is a complication of diabetes that can ultimately lead to vision loss. Early changes of DR include leukocyte... Show moreDiabetic retinopathy (DR) is a complication of diabetes that can ultimately lead to vision loss. Early changes of DR include leukocyte adhesion, pericyte loss, and alterations in retinal blood flow. These changes typically occur prior to clinical diagnosis and can develop into more severe problems such as neovascularization and angiogenesis. The objective of the current study was to investigate retinal hemodynamics in early stages of DR in a diabetic animal model and to evaluate the effect of insulin therapy on retinal hemodynamics in diabetic rats in order to demonstrate how controlled blood glucose levels may regulate changes in vasculature. Lastly, the role of vascular endothelial growth factor (VEGF) on retinal hemodynamics of a normal animal were studied to determine the effects of elevated levels of VEGF on retinal vasculature. Volumetric blood flow (VBF) was quantified using average blood velocity and average diameter measured by using the scanning laser ophthalmoscope (SLO) and the particle tracking method. Pericyte coverage was also quantified with a whole-mount retina technique. In diabetic rats, it was shown that arterial and venous VBF decreased beginning at two weeks post onset of diabetes and continued to decrease throughout the eight week time period. There was no significant loss of pericytes at the eight week time point, however, structural abnormalities were observed at the capillary level. Following insulin therapy, the VBF values of treated diabetic animals were comparable to normal animal VBF values and insulin therapy seemed to normalize VBF of diabetic animals. Exogenous levels of VEGF in normal animals showed significant changes in retinal hemodynamics and vasculature. Future experiments should include investigation of factors that may alter retinal blood flow and quantification of VEGF levels in diabetic animals. Ph.D. in Biomedical Engineering, May 2011 Show less
