Cultured trabecular meshwork (TM) cells are a valuable model system to study the cellular mechanisms involved in the regulation of conventional outflow resistance and thus intraocular pressure; and their dysfunction resulting in ocular hypertension. In this review, we describe the standard procedures used for the isolation of TM cells from several animal species including humans, and the methods used to validate their identity. Having a set of standard practices for TM cells will increase the scientific rigor when used as a model, and enable other researchers to replicate and build upon previous findings.

The eye transduces light, and we usually do not think of it as a biomechanical structure. Yet it is actually a pressurized, thick-walled shell that has an internal and external musculature, a remarkably complex internal vascular system, dedicated fluid production and drainage tissues, and a variety of specialized fluid and solute transport systems. Biomechanics is particularly involved in accommodation (focusing near and far), as well as in common disorders such as glaucoma, macular degeneration, myopia, and presbyopia. In this review, we give a (necessarily brief) overview of many of the interesting biomechanical aspects of the eye, concluding with a list of open problems.

Endothelial NOS overexpression lowers IOP by increasing pressure-dependent drainage in the mouse eye. Data are consistent with NO's having a mechanoregulatory role in aqueous humor dynamics, with eNOS induction at elevated IOPs leading to increased pressure-dependent outflow.

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Evidence suggests that atherogenesis is linked to local hemodynamic factors such as wall shear stress. We investigated the velocity and wall shear stress patterns within a human right coronary artery (RCA), an important site of atherosclerotic lesion development. Emphasis was placed on evaluating the effect of flow waveform and inlet flow velocity profile on the hemodynamics in the proximal, medial, and distal arterial regions. Using the finite-element method, velocity and wall shear stress patterns in a rigid, anatomically realistic model of a human RCA were computed. Steady flow simulations (ReD=500) were performed with three different inlet velocity profiles; pulsatile flow simulations utilized two different flow waveforms (both with Womersley parameter=1.82, mean ReD=233), as well as two of the three inlet profiles. Velocity profiles showed Dean-like secondary flow features that were remarkably sensitive to the local curvature of the RCA model. Particularly noteworthy was the "rotation" of these Dean-like profiles, which produced large local variations in wall shear stress along the sidewalls of the RCA model. Changes in the inlet velocity profiles did not produce significant changes in the arterial velocity and wall shear stress patterns. Pulsatile flow simulations exhibited remarkably similar cycle-average wall shear stress distributions regardless of waveform and inlet velocity profile. The oscillatory shear index was very small and was attributed to flow reversal in the waveform, rather than separation. Cumulatively, these results illustrate that geometric effects (particularly local three-dimensional curvature) dominate RCA hemodynamics, implying that studies attempting to link hemodynamics with atherogenesis should replicate the patient-specific RCA geometry.

The purpose of this work was to investigate the effects of physiologically realistic cardiac-induced motion on hemodynamics in human right coronary arteries. The blood flow patterns were numerically simulated in a modeled right coronary artery (RCA) having a uniform circular cross section of 2.48 mm diam. Arterial motion was specified based on biplane cineangiograms, and incorporated physiologically realistic bending and torsion. Simulations were carried out with steady and pulsatile inflow conditions (mean ReD=233, alpha=1.82) in both fixed and moving RCA models, to evaluate the relative importance of RCA motion, flow pulsation, and the interaction between motion and flow pulsation. RCA motion with a steady inlet flow rate caused variations in wall shear stress (WSS) magnitude up to 150% of the inlet Poiseuille value. There was significant spatial variability in the magnitude of this motion-induced WSS variation. However, the time-averaged WSS distribution was similar to that predicted in a static model representing the time-averaged geometry. Furthermore, the effects of flow pulsatility dominated RCA motion-induced effects; specifically, there were only modest differences in the WSS history between simulations conducted in fixed and moving RCA models with pulsatile inflow. RCA motion has little effect on time-averaged WSS patterns. It has a larger effect on the temporal variation of WSS, but even this effect is overshadowed by the variations in WSS due to flow pulsation. The hemodynamic effects of RCA motion can, therefore, be ignored as a first approximation in modeling studies.

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