Modeling autoregulation in three-dimensional simulations of retinal hemodynamics

Abstract

Purpose: Autoregulation is a mechanism necessary to maintain an approximately constant blood flow rate in the microcirculation when acute changes in systemic pressure occur. Failure of autoregulation in the retina has been associated with various diseases, including glaucoma. In this work, we propose an initial attempt to model autoregulation in a 3D network of retinal arteries.Methods: The blood flow is modeled with the time-dependent Stokes equations. The arterial wall model includes the endothelium and the smooth muscle fibers. Various simplifying assumptions lead to a fluid-structure model where the structural part appears as a boundary condition for the fluid. The numerical simulations are performed on a patient-specific network of 25 segments of retinal arteries located in the inferior temporal quadrant.Results: The simulations performed on the patient-specific artertial network have provided velocities which are in good agreement with published experimental data. In addition, the model allowed to reproduce flow rate-pressure curves which are comparable with experimental data or results obtained with 0D models. In particular, a characteristic plateau of the flow rate has been found for pressures ranging from 40 to 60 mmHg.Conclusion: This work proposes the first 3D simulation of blood flow in a real network of retinal arteries and it also incorporates an autoregulation mechanism. This can be viewed as a first step towards a more complete 3D model of the hemodynamic of the eye.

The Biot-Stokes coupling using total pressure: formulation, analysis and application to interfacial flow in the eye

“…One of the earliest modelling works including a coupling between aqueous humour in the anterior chamber with complying structures is presented in [30], where mechanical properties of the bovine iris were employed to set an elastic interface to represent blinking. Other fluid-structure interaction models have been recently developed in [51], suggesting that flow conditions in the trabecular meshwork and Schlemm's canal could be largely affected by the changes of permeability in microstructure, and [2], where poroelastic properties of the choroid and viscoelastic response of the vitreous body are used to set up a more complete 3D model of larger scale that discards a dedicated physiological description of the trabecular meshwork and considers instead a windkessel model.…”