A Computational Model of Impaired Vasomotion and Retinal Fluid Transport in Diabetic Retinopathy

Abstract

Diabetic retinopathy is associated with early microvascular dysfunction that may alter retinal capillary pressure and promote fluid accumulation in retinal tissue. This study develops a computational model to quantify how the lack of vasomotion affects transcapillary fluid transport and interstitial fluid pressure in the retina. A five-generation retinal arteriole network is first constructed. By introducing vasoconstriction in selected arterioles, the model first simulates the total flow resistance, flow rates, and resulting pressure distribution in the network affected by vasomotion. Starling’s equation was then used to calculate transcapillary fluid filtration, and Darcy’s law was applied to simulate interstitial fluid transport in a cylindrical retinal tissue region. For a simplified two-phase vasomotion cycle, loss of vasomotion increases the average capillary blood pressure by approximately 14%. Over an oscillation cycle, impaired vasomotion increases the required fluid-removal rate at the tissue boundary by approximately 83% in the modeled condition. If the baseline effective retinal fluid-clearance rate is treated as the maximum available clearance capacity, the boundary interstitial pressure must increase by approximately 2.72 mmHg to maintain steady state. Additional simulations examine the effect of increased capillary permeability, which can further enhance fluid leakage into the surrounding tissue. To manage this, the required retinal fluid-clearance rate must increase approximately three- to four-fold, or interstitial fluid pressure must rise by up to 7.52 mmHg. These results suggest that impaired vasomotion may contribute to increased retinal fluid accumulation or elevated interstitial fluid pressure in the retina, and this process may be aggravated as diabetes advances.