###### Abstract  
Trabecular meshwork (TM) motion abnormality is the leading cause of glaucoma. With technique limitations, how TM moves is still an enigma. This study describes a new laboratory platform to investigate TM motion responses to ocular transients in ex vivo eyes. The anterior segments of human cadaver and primate eyes were mounted in a perfusion system fitting. Perfusion needles were placed to establish mean baseline pressure. A perfusion pump was connected to the posterior chamber and generated an immediate transient pressure elevation. A phase-sensitive optical coherent tomography system imaged and quantified the TM motion. The peak-to-peak TM displacements (ppTMD) were determined, a tissue relaxation curve derived, and a time constant obtained. This study showed that the ppTMD increased with a rise in the pulse amplitude. The ppTMD was highest for the lowest mean pressure of 16 mmHg and decreased with mean pressure increase. The pulse frequency did not significantly change ppTMD. With a fixed pulse amplitude, an increase in mean pressure significantly reduced the time constant of recoil from maximum distension. Our research platform permitted quantitation of TM motion responses to designed pulse transients. Our findings may improve the interpretation of new TM motion measurements in clinic, aiding in understanding mechanisms and management. p 2  
in monkeys shows that each waking hour, the eye experiences \(\sim\)10,000 transient IOP fluctuations larger than 0.6 mmHg above the mean baseline pressure with \(\sim\)5000 transient IOP fluctuations greater than 5 mmHg [8,9]. Pulsatile aqueous flow from [PERSON]'s canal (SC) into the episcleral veins occurs in synchrony with the cardiac pulse. Pulsatile cyclic mechanical wall and shear stresses induce signals that confer physiological benefits important to IOP homeostasis. IOP transients also provide forces necessary for the pulsatile discharge of aqueous. In humans, peak-to-peak IOP oscillations with the ocular pulse are about 1.5 mmHg above baseline IOP [5], providing a 3 mmHg pulse amplitude. IOP fluctuations above the baseline of 10 to 14 mmHg occur with saccadic eye movements and with blinking that happens about every 20 s [4]. These oscillatory and transient pressure spikes cause the mobile trabecular meshwork (TM) lamellae to deform outward into SC, which acts as a collapsible chamber. TM distension into SC forces aqueous into collector channels (CC) entrances and aqueous veins. As the pressure spike decays, the TM lamellae return to their original configuration with a resultant reduction of SC pressure, permitting aqueous flow into the canal [10,11]. Pressure-induced deformation of the TM changes SC dimensions, inducing oscillatory pulsations in SC. TM biomechanics determine TM stiffness and the ability to induce pump-like pulsatile flow [11, 12, 13, 14]. Clinical and laboratory evidence has shown that the pulsatile pattern of aqueous flow decreases and even stops in advanced glaucoma, thought to result from increased TM stiffness [10,14]. Optical coherence tomography (OCT) imaging is shedding new light on TM biomechanics. The technology provides unprecedented details of structures, relationships, and motion that provide an evolving picture of functional behavior. OCT coupled with the ability to change pressure gradients in SC [12,15,16], and the anterior chamber (AC) [17] permits studying TM biomechanics under steady-state conditions. However, no technique has been available to measure TM responses to rapid physiological ocular transients. Pulse-transient-induced TM distention has not been studied in the aqueous outflow system, although it has been reported in the prelaminar regions of the optic nerve [18,19]. The time course of TM recoil after transients also remains unknown. The ability of the TM configuration to respond to mean pressure changes and pulse-transients is vital for IOP homeostasis. Loss of TM motion responsiveness to pressure changes might be a crucial factor leading to pressure abnormalities in glaucoma.