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PURPOSE: To evaluate the variations of preretinal oxygen partial pressure (Po2) in normal and in ischemic postexperimental branch retinal vein occlusion (BRVO) areas, during normoxia, hyperoxia (100% O2), and carbogen (95% O2, 5% CO2) breathing before and after intravenous injection of acetazolamide. METHODS: Preretinal Po2 measurements were obtained in intervascular retinal areas, distant from the retinal vessels of 13 anesthetized mini-pigs with oxygen-sensitive microelectrodes (10 μm tip diameter) introduced through the vitreous cavity by a μmanipulator. The microelectrode tip was placed < 50 μm from the vitreoretinal interface in the preretinal vitreous. Po2 was measured continuously for 10 minutes under systemic normoxia, hyperoxia, and carbogen breathing. A BRVO was induced with an argon green laser, and oxygen measurements were repeated under normoxia, hyperoxia, and carbogen breathing, before and after intravenous injection of acetazolamide (500 mg bolus). RESULTS: In hyperoxia, a moderate nonsignificant preretinal Po2 increase in both normal (ΔPo2 = 2.20 ± 4.16 mmHg; n = 25) and ischemic retinas (ΔPo2 = 4.30 ± 3.57 mmHg; n = 16) was measured in spite of a substantial increase in systemic Pao2. Carbogen breathing induced a significant increase in systemic Paco2 and a higher systemic Pao2 than hyperoxia. Furthermore, it significantly increased the preretinal Po2 in normal areas (ΔPo2 = 19.37 ± 16.41 mmHg; n = 26), and in ischemic areas (ΔPo2 = 14.94 ± 8.53 mmHg; n = 14). Intravenous acetazolamide did not affect the preretinal Po2. Acetazolamide induced an increase of the preretinal Po2 to a greater extent when it was associated with carbogen breathing (ΔPo2 = 15.15 ± 9.15 mmHg; n = 7) than when it was combined with hyperoxia (ΔPo2 = 6.96 ± 4.49 mmHg; n = 7). CONCLUSIONS: Carbogen breathing significantly increased preretinal Po2 in normal and in ischemic postexperimental BRVO areas of mini-pigs. The concomitant use of acetazolamide injection and carbogen breathing or hyperoxia could restore an appropriate oxygenation of BRVO areas.
Dr. J.A. Pournaras, Department of Ophthalmology, University Hospital of Geneva, Geneva, Switzerland
10 Differential diagnosis e.g. anterior and posterior ischemic optic neuropathy
11.5 Carbonic anhydrase inhibitors (Part of: 11 Medical treatment)