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J. Pournaras, I.K. Petropoulos, S. Poitry, J. Munoz, C.J. Pournaras; Experimental Branch Retinal Vein Occlusion: Effect of Acetazolamide and Carbogen Breathing (95% O2, 5% CO2) on Preretinal PO2 in Ischemic Areas . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4056.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To evaluate the variations of preretinal PO2 in normal and in ischemic post experimental branch retinal vein occlusion (BRVO) areas, during normoxia, hyperoxia (100% O2), carbogen breathing (95% O2, 5 % CO2), and after intravenous administration of acetazolamide. Methods: Preretinal PO2 measurements were obtained in intervascular retinal areas, far from the retinal vessels of anaesthetized miniature pigs (n=13) with oxygen sensitive microelectrodes (10 µm tip diameter) introduced through the vitreous cavity by a micromanipulator. The microelectrode tip was placed at 50 µm from the vitreoretinal interface in the preretinal vitreous. PO2 was measured continuously during 10 minutes under systemic normoxia, hyperoxia and carbogen breathing. A BRVO was induced with an argon green laser, and oxygen measurements were repeated under these conditions, before and after intravenous injection of acetazolamide (bolus of 500 mg). Results: In hyperoxia, preretinal PO2 remained almost constant in both normal (ΔPO2 = 1.33 mmHg ± 3.39 ; n=13) and ischemic retinas (ΔPO2 = 3.73 mmHg ± 2.84 ; n=8), although systemic PaO2 significantly increased. Carbogen breathing induced a significant increase in systemic PaO2 and PaCO2. Furthermore, it increased significantly the preretinal PO2 in normal and ischemic retinal areas (ΔPO2= 23.05 mmHg ± 17.06 (n=12), and ΔPO2= 22.54 mmHg ± 5.96 (n=6), respectively). Acetazolamide increased PaCO2 and preretinal PO2 only in association with carbogen breathing (ΔPO2 = 15.15 mmHg ± 9.15; n=7). The preretinal PO2 remained elevated even twenty minutes after carbogen breathing had stopped (ΔPO2 = 3.75 mmHg ± 4.42; n=6). Conclusions: In contrast to systemic hyperoxia, carbogen breathing significantly increases preretinal PO2 in normal and in ischemic post experimental BRVO areas of miniature pigs. This effect is probably due to the vasodilation of the retinal arterioles induced by the intravascular PaCO2 increase, leading to a less important decrease in retinal blood flow. The use of acetazolamide injection and carbogen breathing could together restore an appropriate oxygenation of BRVO areas.
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