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1From the Department of Biomedical Sciences, College of Veterinary Medicine, and the 2Department of Zoology and Genetics, Iowa State University, Ames, Iowa; and the 3Department of Ophthalmology and Visual Sciences, University of Iowa Hospitals and Clinics, Iowa City, Iowa.
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 mm Hg/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 PLRratios (indirect/direct PLR) were 76.7 ± 2.6 (mean ± SEM). Twenty-four hours after surgery the PLRratio was 15.2 ± 12.8, 10 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) when compared with the 24-hour postoperative ratios (P < 0.01, repeated-measures ANOVA). Forty-two days after surgery, the PLRratio started to decrease once again in the injured eyes (28.7 ± 5.9). Electroretinographic 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). Histologic 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.
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