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Rasmus Ejstrup, Erik Scherfig, Morten la Cour; Electrophysiological Consequences of Experimental Branch Retinal Vein Occlusion in Pigs and the Effect of Dorzolamide. Invest. Ophthalmol. Vis. Sci. 2011;52(2):952-958. doi: 10.1167/iovs.10-6110.
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To study the electrophysiological consequences of experimental branch retinal vein occlusion (BRVO) in pigs and the effect of dorzolamide.
BRVO was induced in 16 pigs by diathermia. At 4 weeks animals were examined with multifocal electroretinography (mfERG) before and after dorzolamide or vehicle. The direct component P1 (outer retina) and indirect component iN1 (inner retina) were analyzed. Ophthalmoscopy, fundus photography, and fluorescence angiography were performed.
BRVO eyes displayed signs of retinal damage and ischemia on ophthalmoscopy, fundus photography, and fluorescence angiography. mfERGs were affected by surgery; amplitude ratios (BRVO/healthy) were less than one (P1 = 0.30 [0.20–0.45]; iN1 = 0.35 [0.23–0.54]), and implicit time ratios were above one (1.04 [1.03–1.06] and 1.03 [1.02–1.05)]. In healthy eyes, iN1 amplitudes after treatment normalized to baseline (after/before) were lower in dorzolamide-treated animals than in the vehicle group (P = 0.05). After dorzolamide iN1 amplitude ratios (BRVO/healthy) were significantly higher than after vehicle (P = 0.01) and were not significantly different from one (0.97 [0.74–1.26]), indicating that the iN1 amplitudes in BRVO eyes were not different from those in healthy eyes after dorzolamide.
BRVO in pig eyes examined by mfERG is a promising model for testing new treatment strategies in retinal ischemia. The local effects of BRVO are detectable on the mfERG and can be altered by dorzolamide. The decreased iN1 amplitudes caused by dorzolamide in healthy eyes were not seen in BRVO eyes possibly because of an increase in preretinal oxygen tension and improved function of the ischemic retina counteracting the effect of inner retinal acidification.
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