Chapter Eighteen - Intraocular Pressure and the Mechanisms Involved in Resistance of the Aqueous Humor Flow in the Trabecular Meshwork Outflow Pathways
Section snippets
Intraocular Pressure and Aqueous Humor Outflow
Glaucoma, the leading cause of irreversible blindness throughout the world,1 is a chronic, progressive optic nerve neuropathy, in which optic nerve axons are damaged at the optic disc, the site of their exit from the eye. In several prospective randomized multi-center studies, intraocular pressure (IOP) has been identified as the critical causative risk factor for glaucoma and, consequently, the reduction of IOP delays or prevents the damage of optic nerve axons.2, 3, 4, 5, 6, 7, 8 This chapter
Trabecular Meshwork
The trabecular meshwork comprises connective tissue lamellae that are covered by flat, epithelial-like trabecular meshwork cells, which rest on a basal lamina and are of neural crest origin.11, 17 Anteriorly, the trabecular lamellae attach to the peripheral cornea in a region termed Schwalbe's line. Posteriorly, the trabecular lamellae are connected to the stroma of the ciliary body and iris at their junction, and to the scleral spur (Fig. 1). There is considerable evidence that the region
Schlemm's Canal
Schlemm's canal is a modified capillary blood vessel that transiently forms intra- and intercellular pores (Fig. 2), which can acquire unusually large diameters of up to 1 μm.16 As result, the hydraulic conductivity of Schlemm's canal is the highest in the body and even higher than that in the fenestrated capillaries of the glomeruli in the kidney or the sinusoids in the liver.16 Aqueous humor passes Schlemm's canal endothelial cells in a basal-luminal direction, which results in the formation
Outflow Resistance
It is generally accepted that the outflow resistance of the trabecular outflow pathways is localized in the inner wall region comprising the juxtacanalicular tissue and the inner wall endothelium of Schlemm's canal.16 There are three potential mechanisms, which may be involved in the generation of trabecular outflow resistance and which will be discussed here. (1) Outflow resistance largely depends on the quality and quantity of the extracellular matrix in the extracellular spaces of the
Contractile Mechanisms in the Trabecular Outflow Pathways
There are two contractile systems that influence the architecture of the trabecular outflow pathways to modify outflow resistance in the inner wall region. The ciliary muscle is attached to the scleral spur, the posterior attachment of the trabecular meshwork, via tendon-like structures.34, 35 Consequently, contraction of the ciliary muscle results in a changed geometry of the trabecular outflow pathways and reduces outflow resistance in the inner wall region. Experimental disinsertion of
Resistance of the Trabecular Outflow Pathways in Primary Open-Angle Glaucoma
The juxtacanalicular tissue of patients with POAG develops very characteristic structural changes in the course of the disease.44 The quality and quantity of the elastic fibers sheath material in the cribriform plexus changes, and there is an increase of material originally described as “sheath-derived plaques.”45, 46 The increase in the amounts of sheath-derived plaque material in the juxtacanalicular tissue correlates with the severity of optic nerve damage in POAG.47 However, the amount of
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