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I.K. Petropoulos, J.C. Pournaras, J. Munoz, C.J. Pournaras; Effect of Acetazolamide and Carbogen Breathing (95% O2, 5% CO2) on the Optic Disc PO2 . Invest. Ophthalmol. Vis. Sci. 2003;44(13):1298.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose : To evaluate the variations of the optic disc PO2 during normoxia, hyperoxia (100% O2), carbogen breathing (95% O2, 5 % CO2), and after intravenous administration of acetazolamide. Methods : PO2 measurements were obtained at intervascular areas of the optic disc in the intact eyes of anaesthetized miniature pigs (n=11) using oxygen-sensitive microelectrodes (10 µm tip diameter) introduced through the vitreous cavity by an electronic micromanipulator. The microelectrode tip was placed at less than 50 µm from the optic disc. PO2 was measured continuously during 10 minutes under systemic normoxia, hyperoxia and carbogen breathing. Oxygen measurements were repeated under these conditions after intravenous injection of acetazolamide (bolus of 500 mg). Results: In hyperoxia, the optic disc PO2 increased significantly (ΔPO2 = 4.68 ± 2.50 mmHg ; p=0.0001 ; n=11) in parallel with systemic PaO2. Carbogen breathing induced a significant increase in both systemic PaO2 and PaCO2. Furthermore, it increased significantly the optic disc PO2 (ΔPO2 = 16.02 ± 6.15 mmHg ; p<0.0001 ; n=10). Acetazolamide did not affect significantly the PaCO2 and the optic disc PO2, unless carbogen breathing was simultaneously administered (ΔPO2 = 18.91 ± 6.22 mmHg ; p=0.002 ; n=5). In the latter case, the optic disc PO2 was still elevated twenty minutes after the interruption of carbogen breathing (ΔPO2 = 4.27 ± 3.23 mmHg ; p=0.042 ; n=5) in parallel with a high systemic PaCO2. Conclusions: Carbogen breathing increases the optic disc PO2 significantly in miniature pigs more than systemic hyperoxia. Acetazolamide alone is not sufficient to increase the optic disc PO2. The association of acetazolamide injection with carbogen breathing could increase the oxygenation of the optic disc significantly through a postulated vasodilatory effect of elevated systemic PaCO2.
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