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1 General aspects (0)   1.1 Epidemiology (10)   1.2 Population genetics (7)   1.3 Pathogenesis (3)   1.4 Quality of life (3)   1.5 Glaucomas as cause of blindness (2)   1.6 Prevention and screening (5) 2 Anatomical structures in glaucoma (0)   2.1 Conjunctiva (0)   2.2 Cornea (1)   2.3 Sclera (0)   2.4 Anterior chamber angle (0)   2.5 Meshwork (3)     2.5.1 Trabecular meshwork (10)     2.5.2 Schlemms canal (0)     2.5.3 Scleral outlet channels (0)   2.6 Aqueous humor dynamics (0)     2.6.1 Production (0)     2.6.2 Outflow (1)       2.6.2.1 Trabecular meshwork (1)       2.6.2.2 Uveoscleral (0)     2.6.3 Compostion (3)   2.7 Episcleral veins and venous pressure (1)   2.8 Iris (4)   2.9 Ciliary body (3)   2.10 Lens (0)   2.11 Vitreous body (0)   2.12 Choroid, peripapillary choroid, peripapillary atrophy (2)   2.13 Retina and retinal nerve fibre layer (20)   2.14 Optic disc (18)   2.15 Optic nerve (2)   2.16 Chiasma and retrochiasmal central nervous system (1)   2.17 Stem cells (0)   2.20 Other (0) 3 Laboratory methods (2)   3.1 Microscopy (3)   3.2 Electron microscopy (2)   3.3 Immunohistochemistry (8)   3.4 Molecular genetics (2)     3.4.1 Linkage studies (8)     3.4.2 Gene studies (3)   3.5 Molecular biology incl. 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Abstract #9144 Published in IGR 5-2

Functional characterization of retina and optic nerve after acute ocular ischemia in rats

Grozdanic SD; Sakaguchi DS; Kwon YH; Kardon RH; Sonea IM
Investigative Ophthalmology and Visual Science 2003; 44: 2597-2605

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PURPOSE: To functionally characterize the status of the rat retina and optic nerve after acute elevation of intraocular pressure (IOP) and to determine the dynamics of the pathologic changes in the ischemic retina and optic nerve. METHODS: Retinal ischemia was induced in rats by acutely increasing the IOP (110 mmHg/60 minutes). Direct and indirect pupil light reflexes (PLRs) were recorded from the noninjured eye, and electroretinograms (flash and flicker ERG) were recorded from the injured and control eyes before and after surgery. Amplitudes and latencies were calculated for each recording session. RESULTS: Preoperative PLR ratios (indirect/direct PLR) were 76.7 ± 2.6 (mean ± SEM). Twenty-four hours after surgery the PLR ratio was 15.2 ± 12.8, ten days after surgery, 11.6 ± 9.8; 20 days after surgery, 26.5 ± 8.0; and 28 days after surgery, 33.27 ± 9.3. However, at day 35, the PLR had significantly recovered (41.1 ± 7.3) compared to the 24-hour postoperative (p < 0.01, repeated-measures ANOVA) ratio. Forty-two days after surgery, the PLR ratio started to decrease once again in the injured eyes (28.7 ±5.9). Electroretinographical amplitudes (full-field flash ERG) followed a similar pattern. Cone responses (flicker ERG) were measured 42 days after surgery and revealed defects in injured eyes (control eyes: 46.6 ± 2.9 μV, injured eyes: 3.4 ± 1.7 μV). Histological analysis revealed ischemic damage to all retinal layers, with the primary defects localized to the central retina. CONCLUSIONS: Acute ocular ischemia causes a significant decrease in retinal function, as measured by PLR and ERG, although over time the rat retina and optic nerve show partial regain of function.

Dr. S.D. Grozdanic, Department of Biomedical Sciences, College of Veterinary Medicine, , Ames, IA, USA

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Classification:

5 Experimental glaucoma; animal models
6.7 Electro-ophthalmodiagnosis (Part of: 6 Clinical examination methods)

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