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1 From the Department of Ophthalmology and Visual Science, University of Texas-Houston Health Science Center, Houston, Texas; and the 2 College of Optometry, University of Houston, Houston, Texas.
PURPOSE. To investigate the hypothesis that the pathophysiology for the death of retinal ganglion cells in glaucoma involves excitotoxic effects from elevated concentrations of vitreal glutamate.
METHODS. Experimental glaucoma was induced in the right eyes of 18 rhesus monkeys by argon laser treatments to the trabecular meshwork. After significant visual field defects and/or typical clinical glaucomatous changes had developed (1.5–13 months), the eyes were removed, and a sample (0.1–0.2 mL) of posterior vitreous was collected. Similar vitreous samples also were collected from eight untreated monkeys. The vitreous samples were analyzed in a masked fashion by high-pressure liquid chromatography in two independent laboratories. Mean levels of vitreal glutamate were determined for the treated and control eyes and differences between groups of eyes were evaluated by Student’s t-test.
RESULTS. The mean level (± SD) of vitreal glutamate in the eight untreated monkeys was 5.0 ± 2.0 µM. A similar level of 5.7 ± 1.8 µM was measured in the untreated eyes of monkeys with experimental glaucoma. In the glaucomatous eyes, the mean concentration of vitreal glutamate was 5.7 ± 2.6 µM, which was not significantly different from the concentrations in the control eyes.
CONCLUSIONS. Vitreal glutamate concentrations were not elevated in eyes with anatomic and functional damage from experimental glaucoma. This finding is in contradiction to previous reports that vitreal glutamate increases to toxic levels and probably contributes to glaucomatous damage of retinal ganglion cells.
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