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I.K. Petropoulos, J.–L. Munoz, C.J. Pournaras; Metabolic Regulation of the Hypercapnia–Associated Vasodilation of the Optic Nerve Head Vessels . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3908.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: To search for mediators of the hypercapnia–associated vasodilation of the optic nerve head vessels. Prostaglandins and nitric oxide (NO) have been shown to mediate the hypercapnia–associated vasodilation in the retina. Moreover, PO2 measurements are closely associated to local tissue blood flow. Methods: We measured the PO2 at intervascular areas of the optic disc in 17 anaesthetized miniature pigs using oxygen–sensitive microelectrodes placed at less than 50 microns from the optic disc. PO2 was measured continuously during 10 minutes under systemic normoxia, systemic hyperoxia (breathing of 100% O2), carbogen breathing (95% O2, 5% CO2), and hypercapnia (40% increase in inhaled CO2). Similar measurements were also done after intravenous administration of the prostaglandin inhibitor indomethacin (6 animals) or the NO synthase inhibitor L–NAME (6 animals). Results: Before the injections, we observed a slight increase in the optic disc PO2 during hypercapnia (ΔPO2=1.9±1.7 mmHg) as well as during hyperoxia (ΔPO2=3.4±1.6 mmHg), but a much more important increase during carbogen breathing (ΔPO2=12.3±5.2 mmHg). After the injection of indomethacin, the increase in the optic disc PO2 was similar during hyperoxia (ΔPO2=5.6±2.2 mmHg) or carbogen breathing (ΔPO2=5.8±3.2 mmHg). Moreover, the variation of the optic disc PO2 was minimal in hypercapnia after the injection of either indomethacin (ΔPO2=0.5±1.9 mmHg) or L–NAME (ΔPO2=0.7±1.3 mmHg). Conclusions: Indomethacin fully inhibits the vasodilating effect of increased systemic PaCO2 on the optic disc vessels, leading to a similar moderate increase in the optic disc PO2 during carbogen breathing as in hyperoxia. In addition, indomethacin or L–NAME inhibits the increase in the optic disc PO2 seen during hypercapnia. Those results indicate that prostaglandins and, to a lesser extent, NO are mediators of the hypercapnia–associated vasodilation of the optic disc vessels. CO2–induced optic nerve head vasodilation is probably due to a combined effect of prostaglandins and NO.
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