Abstract:
Autoregulation of blood flow, the maintenance of relatively constant blood flow despite variations in pressure, is characteristic of many tissues, including the retina. Impaired retinal autoregulation has been shown to be a risk factor for glaucoma, suggesting that the relation between vascular regulatory mechanisms and glaucoma progression should be investigated. In this study, a vascular wall mechanics model is used to predict the relative importance of regulatory mechanisms in achieving retinal autoregulation. Five segments, connected in series, represent the following classes of vessels downstream of the central retinal artery: large arterioles, small arterioles, capillaries, small venules, and large venules. The large and small arterioles respond actively to local changes in pressure, shear stress, and carbon dioxide and to the downstream metabolic state communicated via conducted responses. Model parameters governing wall tension are fit to pressure and diameter data from porcine retinal arterioles. The model is able to predict the range of pressures for which autoregulation is achieved for both control and elevated levels of intraocular pressure. The model results indicate a shift in the autoregulation range when IOP is increased. A key role for metabolic responses in attaining retinal autoregulation is also predicted.