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Effect of Systemic Nitric Oxide Synthase Inhibition on Optic Disc Oxygen Partial Pressure in Normoxia and in Hypercapnia

¹From the Laboratory of Ocular Vascular Diseases, Faculty of Medicine, University of Geneva, Geneva, Switzerland; and the ²Jules Gonin Eye Hospital, University of Lausanne, Lausanne, Switzerland.

PURPOSE. To investigate the effect of systemic nitric oxide synthase (NOS) inhibition on optic disc oxygen partial pressure (PO₂) in normoxia and hypercapnia.

METHODS. Intervascular optic disc PO₂ was measured in 12 anesthetized minipigs by using oxygen-sensitive microelectrodes placed <50 µm from the optic disc. PO₂ 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-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 PO₂ during hypercapnia (PO₂ = 3.2 ± 1.7 mm Hg; 18%; P = 0.001) and carbogen breathing (PO₂ = 12.8 ± 5.1 mm Hg; 69%; P < 0.001). Optic disc PO₂ 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 PO₂ increase under hypercapnia was blunted after L-NAME injection (PO₂ = 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% (PO₂ = 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 PO₂ in normoxia, a blunting effect was noted on the CO₂-induced optic disc PO₂ increase. Nitric oxide appears to mediate the hypercapnic optic disc PO₂ increase.