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Effect of Indomethacin on the Hypercapnia-Associated Vasodilation of the Optic Nerve Head Vessels: An Experimental Study in Miniature Pigs

Purpose: To evaluate whether prostaglandins are mediators of the hypercapnia-associated vasodilation of the optic nerve head vessels. Methods: We measured the PO2 at intervascular areas of the optic disc in 9 anaesthetized miniature pigs using oxygen-sensitive microelectrodes placed at <50 µm from the optic disc. PO2 was measured continuously under normoxia, hyperoxia (breathing of 100% O2), carbogen breathing (95% O2, 5% CO2), and hypercapnia (40% increase in inhaled CO2). Similar measurements under these conditions were also done after intravenous administration of the prostaglandin inhibitor indomethacin. Results: Before the injection of indomethacin, we observed a slight increase in the optic disc PO2 during hypercapnia (ΔPO2 = 2.0 ± 1.7 mm Hg; p < 0.001; n = 18) or hyperoxia (ΔPO2 = 3.4 ± 1.6 mm Hg; p < 0.001; n = 23), but a much more important increase during carbogen breathing (ΔPO2 = 12.0 ± 5.1 mm Hg; p < 0.001; n = 23). After the injection of indomethacin, the increase in the optic disc PO2 was similar during hyperoxia (ΔPO2 = 5.6 ± 2.2 mm Hg; p < 0.001; n = 9) or carbogen breathing (ΔPO2 = 5.8 ± 3.2 mm Hg; p < 0.001; n = 9), while in hypercapnia the variation of the optic disc PO2 was minimal (ΔPO2 = 0.5 ± 1.9 mm Hg; p > 0.1; n = 6). Conclusions: Indomethacin inhibits the vasodilatory effect of increased systemic PaCO2 on the optic nerve head vessels, leading to a similar moderate increase in the optic disc PO2 during carbogen breathing as in hyperoxia. Indomethacin also inhibits the increase in the optic disc PO2 seen during hypercapnia. Those results indicate that prostaglandins are mediators of the hypercapnia-associated vasodilation of the optic nerve head vessels.