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Ioannis K. Petropoulos, Jean-Antoine C. Pournaras, Alexandros N. Stangos, Constantin J. Pournaras; Effect of Systemic Nitric Oxide Synthase Inhibition on Optic Disc Oxygen Partial Pressure in Normoxia and in Hypercapnia. Invest. Ophthalmol. Vis. Sci. 2009;50(1):378-384. doi: 10.1167/iovs.08-2413.
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purpose. To investigate the effect of systemic nitric oxide synthase (NOS) inhibition on optic disc oxygen partial pressure (Po 2) in normoxia and hypercapnia.
methods. Intervascular optic disc Po 2 was measured in 12 anesthetized minipigs by using oxygen-sensitive microelectrodes placed <50 μm from the optic disc. Po 2 was measured continuously during 10 minutes under normoxia, hyperoxia (100% O2), carbogen breathing (95% O2, 5% CO2), and hypercapnia (increased inhaled CO2). Measurements were repeated after intravenous injection of N ω-nitro-l-arginine methyl ester (l-NAME) 100 mg/kg. Intravenous l-arginine 100 mg/kg was subsequently given to three animals.
results. Before l-NAME injection, an increase was observed in optic disc Po 2 during hypercapnia (ΔPo 2 = 3.2 ± 1.7 mm Hg; 18%; P = 0.001) and carbogen breathing (ΔPo 2 = 12.8 ± 5.1 mm Hg; 69%; P < 0.001). Optic disc Po 2 in normoxia remained stable for 30 minutes after l-NAME injection (4% decrease from baseline; P > 0.1), despite a 21% increase of mean arterial pressure. Optic disc Po 2 increase under hypercapnia was blunted after l-NAME injection (ΔPo 2 = 0.6 ± 1.1 mm Hg; 3%; P > 0.1), and this effect was reversible by l-arginine. Moreover, l-NAME reduced the response to carbogen by 29% (ΔPo 2 = 9.1 ± 4.4 mm Hg; 49%; P = 0.01 versus before l-NAME). The response to hyperoxia was not affected.
conclusions. Whereas systemic NOS inhibition did not affect optic disc Po 2 in normoxia, a blunting effect was noted on the CO2-induced optic disc Po 2 increase. Nitric oxide appears to mediate the hypercapnic optic disc Po 2 increase.
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