Abstract
We propose an integrated model of aqueous outflow control that employs a pump-conduit system in this article. Our model exploits accepted physiologic regulatory mechanisms such as those of the arterial, venous, and lymphatic systems. Here, we also provide a framework for developing novel diagnostic and therapeutic strategies to improve glaucoma patient care. In the model, the trabecular meshwork distends and recoils in response to continuous physiologic IOP transients like the ocular pulse, blinking, and eye movement. The elasticity of the trabecular meshwork determines cyclic volume changes in Schlemm’s canal (SC). Tube-like SC inlet valves provide aqueous entry into the canal, and outlet valve leaflets at collector channels control aqueous exit from SC. Connections between the pressure-sensing trabecular meshwork and the outlet valve leaflets dynamically control flow from SC. Normal function requires regulation of the trabecular meshwork properties that determine distention and recoil. The aqueous pump-conduit provides short-term pressure control by varying stroke volume in response to pressure changes. Modulating TM constituents that regulate stroke volume provides long-term control. The aqueous outflow pump fails in glaucoma due to the loss of trabecular tissue elastance, as well as alterations in ciliary body tension. These processes lead to SC wall apposition and loss of motion. Visible evidence of pump failure includes a lack of pulsatile aqueous discharge into aqueous veins and reduced ability to reflux blood into SC. These alterations in the functional properties are challenging to monitor clinically. Phase-sensitive OCT now permits noninvasive, quantitative measurement of pulse-dependent TM motion in humans. This proposed conceptual model and related techniques offer a novel framework for understanding mechanisms, improving management, and development of therapeutic options for glaucoma.
Highlights
Glaucoma is a leading cause of irreversible blindness resulting in optic nerve damage and visual field loss (Susanna et al, 2015)
The tethering of s canal (SC) endothelium to trabecular meshwork (TM) lamellae via cytoplasmic processes ensures that when the TM moves outward into the SC lumen, the lamellae can limit the sheet of SC endothelial cells distention into the canal
The type C tendons form a network of elastic-like fibers that provide connections extending from the ciliary muscle tendons to the trabecular lamellae, juxtacanalicular cells, and SC inner wall endothelium
Summary
Glaucoma is a leading cause of irreversible blindness resulting in optic nerve damage and visual field loss (Susanna et al, 2015). An accurate understanding of mechanisms controlling IOP can lead to improvements in the treatment of the disease. Objective clues to the nature of aqueous outflow are evident in humans, in whom we can directly see the return of aqueous humor to the episcleral veins. An important observation is that flow into the episcleral veins is pulsatile, indicating the existence of a vascular pump. Pulsatile aqueous outflow diminishes and eventually stops in glaucoma patients (Ascher, 1961). These observations should not be overlooked, and it seems important that they are integrated into any theoretical framework explaining aqueous outflow. Pulsatile aqueous outflow behavior provides a framework for inte grating structural and functional evidence into our 21st-century concept of aqueous outflow. We charac terize this phenomenon in health and disease in the hope that it will lead to a better understanding of the disease process’s pathophysiology, diagnosis, and treatment
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