Blood Aqueous Barrier

The blood-aqueous barrier restricts the penetration of solutes such as acri-flavine (MW 540) into the posterior chamber as well as the anterior chamber (Rodriguez-Peralta, 1975). With the blood-aqueous barrier, inward movement of solutes from the blood to the eye is more restrictive compared to the outward movement. The blood-aqueous barrier is principally constituted by two discrete layers of cells: the endothelium of the iris and ciliary blood vessels and the nonpigmented ciliary epithelium. To pass from the blood vessels of iris into the posterior chamber, a substance has to cross the iris vessels, the stroma, a layer of iris muscle, and the iris epithelium. Transport from the stroma into the anterior chamber is easier because the cellular layer on the anterior surface of the iris is incomplete. In the anterior chamber angle, there is continuous drainage of aqueous humor, which limits the movement of solutes from the anterior chamber to posterior chamber. To pass from the blood vessels of the ciliary body into the posterior chamber, a solute has to cross the ciliary microvessels, the loose connective tissue of the stroma, and the two-layered ciliary epithelium. The capillaries of the iris have a relatively thick wall layered by the continuous-type endothelial cells that are attached to each other by tight junctional complexes (Raviola, 1977; Freddo and Raviola, 1982). The number of strands in the zonulae occludens of these cells in the monkey varies from one to eight. As in the blood-brain barrier (BBB), GLUT-l and P-glycoprotein are present in iris and ciliary vessel endothelial cells, while endothelial antigen PAL-E (Pathologische Anatomie Leiden-Endothelium) and the transferrin receptor are absent (Schlingemann et al., 1998). This suggests a phenotypic similarity of iris and ciliary vessels with brain microvessels. The iris vessels restrict the transport of circulating horseradish peroxidase (HRP) and fluorescein due to the presence of tight junctions between the endothelial cells. In this regard, the vessels of the iris, retina, and brain share a common behavior (Hank et al., 1990; Holash and Stewart, 1993; Stewart and Tuor, 1994). However, ciliary vessels are permeable to circulating HRP, and it is speculated that it reaches ciliary muscle by diffusion from the permeable vessels of the ciliary processes.

The ciliary body epithelium is made of an outer pigmented epithelium (PE) and an inner nonpigmented epithelium (NPE) juxtaposed at their apical surfaces (Fig. 6). The tight junctions between NPE cells impose a diffusion barrier between blood and aqueous humor (Schlingemann et al., 1998). Intravenously injected HRP passes through the fenestrated ciliary endothe-lial cells and reaches the intercellular spaces around PE cells and those between PE and NPE cells. However, the tight junctions at the apico-lateral

Figure 6 Putative ion and solute transport processes in the mammalian pigmented and nonpigmented epithelial cells of the ciliary body.

fusion points of the NPE cells block further movement of HRP into the posterior chamber (Schlingemann et al., 1998). Gap junctions are ubiquitous in the ciliary body epithelium, connecting PE-to-PE, NPE-to-NPF, and PE-to-NPE cells (Freddo, 1987) (Fig. 6). The gap junctions between PE and NPE cells are permeable to molecules at least as large as 900-1000 daltons (Spray and Bennett, 1985).

In general, the breakdown of the blood-aqueous barrier takes place when the mammalian eye is subjected to painful or irritant stimuli in response to mechanical trauma or by carotid infusion of hyperosmotic agents, leading to the leakage of plasma proteins into the aqueous humor (Butler et al., 1988). This breakdown may be due to shrinkage of the pigmented epithelial cells, degeneration of the junctional complexes, and separation of the two epithelial cell layers. In addition, stimulation of ocular motor nerve, local administration of prostaglandin (PGE 1), and systemic injection of a-MSH causes dilatation of iris and ciliary capillaries and relaxation of afferent vessels, leading to the disruption of the blood-aqueous barrier.

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