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.
Highlights
Glaucoma is a leading cause of irreversible blindness in the world [1]
The findings indicate that changes in peak-to-peak TM displacements (ppTMD) induced by baseline and pulsatile changes in Intraocular pressure (IOP) reflect increases in stiffness in response to stepwise increases in pressure
Our study found that the Trabecular meshwork (TM) shows viscoelastic behavior, though the viscous effects are very small under an ocular pulse of ≤5 mmHg at all baseline IOP levels
Summary
Glaucoma is a leading cause of irreversible blindness in the world [1]. Intraocular pressure (IOP) elevation is widely accepted as a major cause and the only treatable factor for POAG [2,3]. Many IOP transients occur over a day in response to the ocular pulse [4,5,6], blinking, and eye movements [4,7]. Pulsatile aqueous flow from Schlemm’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 provide forces necessary for the pulsatile discharge of aqueous
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