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Y Ito, J Liggett, B Berkowitz; Temporal Evolution of the Retinal Oxygenation Response Following Acutely Elevated Intraocular Pressure in a Rat Model . Invest. Ophthalmol. Vis. Sci. 2002;43(13):310.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Retinal blood flow is known to decrease after transient global retinal ischemia (ligated optic nerve) in the rat. In the present study, we test the hypothesis that the retinal oxygenation response also decreases in a different transient retinal ischemia rat model. Methods: Sprague-Dawley rats (n = 7) were anesthetized with urethane and retinal ischemia was induced for 60 minutes with high intraocular pressure (>150mmHg, IOP). IOP was then brought back to normal (15 mm Hg). A novel functional magnetic resonance imaging (fMRI) method was used to determine the preretinal vitreous oxygenation response (Δ;PO2, mm Hg) to a carbogen (95% O2 : 5%CO2) inhalation challenge. In each animal, Δ;PO2 was measured before ischemia, during ischemia, and during reperfusion (15, 30, 45, 60, 75 and 90 min). Results: Δ;PO2 before and during ischemia was 124 4mmHg (mean SEM) and 28 3 mmHg, respectively. During reperfusion, Δ;PO2's were 236 9 (15 min), 150 5 (30 min), 147 7 (45 min), 137 8 (60 min), 164 10 (75 min), and 142 7 (90 min). Preretinal Δ;PO2 15 and 30 min after ischemia was significantly higher than Δ;PO2 before ischemia (P < 0.05). Conclusion: The reason for the dramatic increase in oxygenation 15-30 min following ischemia is not known. We speculate that suppression of photoreceptor function during reperfusion allowed oxygen from the choroid to reach the preretinal vitreous.
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