Within the eyeball are three chambers: the anterior chamber (camera anterior bulbi), the posterior chamber (camera posterior bulbi), and the vitreous chamber (camera vitrea bulbi).
The anterior chamber is the space bounded by the cornea anteriorly and the iris and anterior lens surface posteriorly. It is filled with the aqueous humor. The anterior chamber is in direct communication with the posterior chamber through the aperture of the iris. The periphery of the chamber is continuous with the spaces of the iridocorneal angle.
The posterior chamber is smaller than the anterior chamber, being approximately 50% of the latter in volume. It is bounded anteriorly by the iris, posteriorly by the lens capsule and anterior face of the vitreous, and peripherally by the zonule and ciliary epithelium.
Aqueous humor fills the anterior and posterior chambers. The humor is produced by an active secretory process from the epithelium (pars ciliaris retinae) of the richly vascular ciliary body. The mean volume of aqueous humor is 1.7 (±0.86) mL in the dog. The aqueous is normally clear and colorless. It is very low in protein compared with blood plasma and more closely resembles the cerebrospinal fluid in composition than any other fluid formed in the body. Normally the aqueous humor is maintained at an intraocular pressure of approximately 17 to 21 mm Hg in the dog. This pressure is essential to maintain the normal shape and firmness of the eyeball. When the intraocular pressure is lost postmortem or as a result of the escape of aqueous humor through a corneal laceration, the eye becomes soft and deformed.
The conventional pathway for aqueous outflow in the dog has been described by Samuelson and Gelatt (1984). The aqueous humor flows from its site of production, the epithelium of the ciliary processes, into the posterior chamber, through the pupil into the anterior chamber and peripherally to the intertrabecular spaces of the iridocorneal angle. Here it is resorbed into the blood stream by the angular aqueous plexus. A second, unconventional, uveoscleral pathway for aqueous drainage has recently been described in a variety of species. In the uveoscleral route, aqueous humor leaves the anterior chamber, passes caudally through the uveal trabecular meshwork and tendinous attachments of the anterior ciliary body musculature, percolates through the meridional ciliary body muscle, and enters the supraciliary and suprachoroidal spaces. The fluid is then absorbed by the choroidal and scleral circulation. This route has been shown to account for approximately 15% of total aqueous outflow in the normal dog and to be markedly diminished, accounting for only 3% of total outflow in glaucomatous Beagles. The trabecular meshwork and aqueous outflow channels are innervated with sympathetic axons, suggesting a neural influence on aqueous dynamics.The trabecular meshwork cells within the iridocorneal angle contain smooth muscle actin and contraction is likely to alter aqueous outflow. A delicate balance between production and resorption maintains the normal intraocular pressure. The production of aqueous humor is not regulated by the intraocular pressure. Canine uveoscleral tissue demonstrates high succinic dehydrogenase and lactic dehydrogenase activity. Although this may suggest greater metabolic activity in this tissue, the importance of these enzymes for the outflow of aqueous humor is unknown. Occlusion of the primary outflow pathway, either at the pupil or iridocorneal angle, results in an increase in intraocular pressure (glaucoma) leading to optic neuropathy, retinal atrophy, and blindness.
Elevated levels of endothelin-1, nitric oxide, and glutamate are associated with various forms of glaucoma. The mean concentration of endothelin-1, nitric oxide, and glutamate in the aqueous humor of normal dogs is 3.05 pg/mL, 4.12 µm and 2.35 µm, respectively.
The topical application of angiotensin-converting enzyme inhibitors decreases intraocular pressure; however, the role of angiotensin-converting enzyme in the normal canine eye remains unclear. Age-related vitreous degeneration, especially mild vitreal syneresis, is not an uncommon finding in normal dogs.
The vitreous chamber is the largest of the three chambers of the eye, accounting for approximately 80% of the volume of the eyeball. The zonule and posterior lens capsule form the anterior limit of the chamber. The retina encloses the remainder.
The vitreous body occupies the vitreous chamber. The vitreous body is a soft, clear gel, which conforms to the shape of the cavity it occupies. Thus the anterior face of the vitreous is indented (fossa hyaloidea) by the posterior face of the lens. Similarly, the surface of the vitreous is fluted where it projects anteriorly between the ciliary processes.
The vitreous body is almost entirely acellular. The bulk of the vitreous is formed by the liquid component (humor vitreus), a solution of mucopolysaccharides rich in hyaluronic acid. The vitreous body is composed of approximately 98% water and 2% solids. Among the solids, proteins are the major constituents (88%) followed by lipids (9%) and carbohydrates (4%). Although the canine vitreous body is classically considered to be an inert structure, recent studies have documented that it is metabolically active. The structure of the vitreous is reinforced by fibers of vitrein (stroma vitreum), which consists of collagen type II and are essential to its gel characteristics. Vitrein fibers are especially numerous near the ora ciliaris retinae but do not lend sufficient rigidity to maintain the shape of the vitreous after its removal from the eye. Fine and Yanoff (1972) have aptly described the vitreous as the “most delicate of all the connective tissue in the body.” The anterior face of the vitreous is limited by the membrana vitrea. This is not a discretely demonstrable membrane in the ordinary sense but rather a local condensation of the filamentous framework found throughout the vitreous. In humans it is of sufficient strength to contain the vitreous after removal of the lens and lens capsule via the hyaloid-lenticular ligament. In the dog, intracapsular lens removal is impractical because the vitreous membrane is thin and tightly adherent to the posterior lens capsule. Attempts to remove the lens within its capsule usually result in tearing of the vitreous face with subsequent loss of the vitreous body.
The vitreous body is also tightly adherent to the pars ciliaris retinae at the ora ciliaris retinae and to the optic disc, as well as to the posterior lens capsule. In the adult dog it is easily separated from the retina except at these points.
Elevated levels of endothelin-1, nitric oxide, and glutamate are associated with various forms of glaucoma. The concentration of endothelin-1, nitric oxide, and glutamate in the vitreous of normal dogs is 1.83 pg/mL, 4.86 µm and 1.37 µm, respectively.
The hyaloid canal (canalis hyaloideus) traverses the vitreous from the optic disc to the posterior face of the lens. It is the funnel-shaped remnant of the primary (embryologic) vitreous. As the secondary or definitive vitreous is elaborated by the retina, the primary vitreous is compressed centrally. At the same time, the primary vitreous is attenuated by being stretched as the globe increases in size. The hyaloid canal is broadest anteriorly, where it is attached to the posterior surface of the lens. The attachment to the lens can be visualized with the biomicroscope as a thin, white circle approximately 3 mm in diameter surrounding the posterior pole of the lens. The canal tapers posteriorly toward the optic disc and usually exhibits an inferior sag between its points of attachment; the hyaloid canal is concave superiorly in most dogs. The primary vitreous is normally of the same optical clarity as the rest of the vitreous body and can be distinguished only by a slight difference in optical refractivity resulting from local differences in the vitreous stroma. With the appropriate illumination, a line of demarcation can be detected at the interface of the primary and secondary vitreous (the “wall” of the canal). Occasionally, hemorrhage into the vitreous spreads along the interface, clearly outlining the canal.
In the embryo, the hyaloid artery courses through the hyaloid canal from the optic disc to the lens to supply the posterior surface of the growing lens. This artery normally atrophies completely by the time the eyelids open; a small white dot on the posterior pole of the lens marks its site of attachment. The multilayered fenestrated sheaths peculiar to the fine structure of the primary vitreous probably derive from the tunica media of the hyaloid vessels. Remnants of the artery itself are occasionally seen ophthalmoscopically, especially in very young dogs. Rarely, persistent hyaloid arteries occur and result in posterior lenticular cataracts. The vitreous degenerates with age and its breakdown can be detected more effectively by ultrasonography than by ophthalmoscopy.