No abstract

Retinal damage in dogs with PG differs in intensity in focal areas. Damage in affected regions resembles damage induced by glutamate. Glutamate is lost from damaged neurons and accumulates in Müller cells, which is consistent with increased glutamate release contributing to the damage. Glutamate antagonists may protect INL cells in dogs with glaucoma.

The clinical work-up, diagnosis and follow-up of an 8-year-old, female-spayed Shih Tzu with diffuse, granulomatous meningoencephalomyelitis (GME)-causing visual deficits is reported. The use of cytosine arabinoside as an alternative treatment for GME is discussed.

Retinal damage in dogs with PG includes ischemia-like losses of taurine and glutamate from photoreceptors and accumulation of glutamate, but not taurine, in nearby Müller cells. These changes are consistent with glutamate release and depletion of intracellular taurine in damaged regions, perhaps contributing to progressive damage in these areas.

Ultrasound biomicroscopy was performed on enucleated feline globes as a model for use in vivo. Quantitative measurements were obtained from the anterior segment using a 50-MHz transducer. Mean values from 26 feline globes were axial corneal thickness, 0.74 mm; anterior chamber depth, 4.20 mm; distance from the first ciliary process to the limbus, 3.17 mm; angle recess, 0.38 mm; angle opening distance, 1.05 mm; iris base width 0.38 mm; iris middle width 0.52 mm; iris tip width 0.13 mm, and iris-lens overlap, 0.69 mm. Distinctive features of the feline anterior segment include a relatively wide iridocorneal angle and deep anterior chamber.

Decreases in GS immunoreactivity were associated with glutamate redistribution. These decreases in GS occurred even in mildly damaged regions of retina before retinal thinning. Reactive Müller cells were seen primarily in chronic PG in severely damaged regions. Decreases in GS may potentiate ischemia-induced early glutamate redistribution and neuronal damage in canine PG.

Microvessel loss may occur in regions of glutamate redistribution and neuronal damage in PG retinas. Larger vessels were often damaged. The redistribution of glutamate is associated with a loss of microvessels, even in mildly damaged regions. However, neuronal damage and glutamate redistribution may occur close to remaining microvessels, suggesting microvessel loss was not the sole factor inducing these changes.

The relationship between AOD as measured by UBM pre-operatively is weakly associated with IOP pressure elevations at day one post-phacoemulsification. Further study is required prospectively to establish the importance of this relationship. Initial measurements of the canine iridocorneal angle were created, suggesting a method to be used in the future to establish true canine normal measurements.