Modeling the impact of venous collapsibility on retinal oxygenation

Glaucoma is a leading cause of blindness worldwide that is characterized by progressive and irreversible vision loss. In addition to elevated intraocular pressure (IOP), impairments in retinal blood flow and oxygen (O₂) metabolism contribute to the pathophysiology of glaucoma. In this study, a theoretical model of the retinal vasculature is expanded to allow for venous collapsibility. The model also accounts for mechanistic flow regulation and O₂ transport and is used to predict retinal blood flow and tissue oxygenation as intraluminal pressure, O₂ demand, or IOP are varied. Venules are represented as Starling resistors to allow for venous collapsibility when the external pressure is higher than the internal vascular pressure. At elevated levels of IOP, simulations are conducted when venous collapsibility is present and when venules are considered fixed resistors. At baseline IOP, blood flow remains relatively constant (i.e., an autoregulation plateau occurs) for a pressure range of 32–43 mmHg. The plateau is shifted to a significantly higher pressure range of 39–50 mmHg when IOP is elevated with venous collapsibility, indicating that the capacity for autoregulation is reduced at physiological pressures. Correspondingly, resistance in the venules is increased with elevated IOP but remains constant when venules are treated as fixed resistances. Additionally, when IOP is elevated and collapsibility is present, the increase in flow with O₂ demand is significantly reduced. Ultimately, the model framework provides for future comparisons with sectorial-specific clinical data to help assess the potential role of impaired blood flow regulation in ocular disease.