## 4 Discussion  
This study demonstrates our research platform's ability to explore TM motion responses to intraocular pulse transients in human and nonhuman primate eyes. Pulse transients are a crucial component of the forces the TM experiences because blinking and eye movement are frequent [9]. Studying responses to transient ocular spikes can provide insights into the normal TM tissue biomechanical properties and provide a means to compare the findings with those of glaucoma patients. Our PhS-OCT study is limited to measuring bulk responses of the trabecular beams because the resolution is not adequate to assess the movement of smaller structural features  
Figure 4: The mean and standard deviation of the peak-to-peak trabecular meshwork displacement (ppTMD) from applying various mean pressures, pulse amplitudes, and pulse frequencies. A different color specifies each pulse frequency, and each data point is the average of 4 measurements. Macaca Nemestrina Eye. Figure 5: The mean and standard deviation of trabecular meshwork recoil time constant for (**A**) humans and (**B**) nonhuman primates (Macaca Nemestrina). IOP: intraocular pressure. Each graph normalized all values to the 16 mmHg IOP and 2.5 mmHg pulse amplitude (i.e., first black bar). * indicates significant differences between groups. Each data point is the average of 4 measurements. such as SC inner wall endothelium [20]. In vivo, IOP induces a constant loading force or prestress on the TM tissues [10; 12]. SC is a compressible chamber, and IOP loading forces continuously drive the TM tissues outward toward SC external wall, tending to reduce the relative size of the chamber lumen. [PERSON]'s line anteriorly combined with the scleral spur and ciliary body posteriorly anchor the TM between the AC and SC. Ciliary body tension and elastance of the trabecular beams determine the ability of the TM to maintain its optimal position suspended in 3D space between the AC and the canal. Elastance, also called stiffness, is the property that determines the ability of a tissue to store elastic energy controlling the ability to distend and recoil [12; 21; 22]. The loading force of IOP causes stresses that induce TM strain. TM strain deformation causes the SC lumen to narrow. The IOP loading force on the TM must be constantly balanced by the combined forces of ciliary muscle tension and trabecular lamellar elastance. In the absence of optimized elastance, the TM would distend into SC, resulting in persistent canal closure and occlusion of collector channel entrances. SC collapse is widely recognized by clinical and laboratory studies as a causal factor resulting in increased resistance in glaucoma [23; 24]. Drugs such as pilocarpine increase ciliary body tension, increasing the tensile load, thereby altering the TM elastance/stiffness. The altered elastance increases pulsatile aqueous outflow and reduces pressure in glaucoma patients [25; 26]. Such considerations emphasize the clinical importance of understanding the mechanics of the TM tissues. When we induce an experimental pulse amplitude increase, the ppTMD markedly increases at each of the mean pressures tested in both the human and NHP eyes (Figure 3). For example, at a mean pressure of 16 mmHg, ppTMD rose from 0.3 \(\upmu\)m to 1.6 \(\upmu\)m, demonstrating a profound effect of pulse amplitude on ppTMD. Increases in baseline IOP decreased the ppTMD pulse amplitude response (Figure 3). At a pulse amplitude of 2.5 mmHg, minimal differences were present at a baseline IOP of 16 mmHg. However, the relative ppTMD markedly decreased as baseline IOP increased. The baseline IOP of 32 and 40 mmHg reduced ppTMD by 50% or more compared with the 16 mmHg baseline IOP in both the human and NH primate eyes. The ppTMD was affected by both baseline IOP and pulse amplitude, indicating that the TM shows a nonlinear force-displacement relationship (hyperelastic) that is typical in ocular tissues. Specifically, at a relatively lower baseline IOP, the TM's stiffness is lower than that of a higher baseline IOP.