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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(omega)-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 (DeltaPO2 = 3.2 ± 1.7 mmHg; 18%; P = 0.001) and carbogen breathing (DeltaPO2 = 12.8 ± 5.1 mmHg; 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 (DeltaPO2 = 0.6 ± 1.1 mmHg; 3%; P > 0.1), and this effect was reversible by L-arginine. Moreover, L-NAME reduced the response to carbogen by 29% (DeltaPO2 = 9.1 ± 4.4 mmHg; 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.
Dr. I.K. Petropoulos, Laboratory of Ocular Vascular Diseases, Faculty of Medicine, University of Geneva, Geneva, Switzerland
6.11 Bloodflow measurements (Part of: 6 Clinical examination methods)
3.8 Pharmacology (Part of: 3 Laboratory methods)
2.14 Optic disc (Part of: 2 Anatomical structures in glaucoma)