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D. O. Zamora, A. L. Maldonado, J. W. Kiel; Hyperoxia Treatment Reverses the Effects of L-NAME on Aqueous Flow. Invest. Ophthalmol. Vis. Sci. 2008;49(13):352.
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We previously reported that nitric oxide synthase inhibition with L-NAME causes ciliary vasoconstriction and decreased aqueous production. We proposed that L-NAME inhibition of aqueous production is due to reduced oxygen delivery. The present study tested this hypothesis by respiring animals with 100% oxygen after giving L-NAME.
In pentobarbital anesthetized rabbits (n=16, 2.3 ± 0.1 kg) direct cannulation was used to measure mean arterial pressure (MAP), intraocular pressure (IOP), and orbital venous pressure (OVP). Carotid blood flow was measured by transit time ultrasound (BFcar, Transonic Systems TS420), heart rate (HR) by a digital cardiotachometer, ciliary blood flow by laser Doppler flowmetry (BFcil, Perimed PF 5000), and aqueous flow by fluorophotometry (Flow, Ocumetrics FM2). The protocol entailed 60 min of baseline recording, then L-NAME (5 mg/kg, iv) was given, and the recording continued for 180 min with the animals respired with room air (n=5) or 100% O2 (n=11) for the last 90 min.
In both groups, L-NAME increased MAP as well as ciliary and carotid vascular resistance and decreased HR, IOP and Flow. Hyperoxia increased Flow such that it was not significantly less than control; continued normoxia did not alter Flow.
Hyperoxia treatment partially reverses the effect of L-NAME on aqueous production. The data support the broader hypothesis that adequate oxygen delivery by the ciliary circulation is essential for aqueous production.
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