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Karl-Heinz Huemer, Gerhard Garhofer, Tina Aggermann, Julia Kolodjaschna, Leopold Schmetterer, Gabriele Fuchsjäger-Mayrl; Role of Nitric Oxide in Choroidal Blood Flow Regulation during Light/Dark Transitions. Invest. Ophthalmol. Vis. Sci. 2007;48(9):4215-4219. doi: 10.1167/iovs.07-0176.
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purpose. Several studies have recently shown that a transition from light to dark is associated with a reduction in choroidal blood flow. The mechanism underlying this effect is unclear but may be related to changes in neural input. In the present study, the authors hypothesized that either the α-receptor agonist phenylephrine or the nitric oxide synthase (NOS) inhibitor L-NMMA may alter the choroidal blood flow response during a transition from light to dark.
methods. In 15 healthy male nonsmoking subjects, the response of choroidal perfusion was studied in a randomized placebo-controlled three-way crossover study. Phenylephrine, L-NMMA or placebo was administered on different study days, and the effect of a light/dark transition on choroidal perfusion parameters was studied. Subfoveal choroidal blood flow and fundus pulsation amplitude were assessed with laser Doppler flowmetry and laser interferometry, respectively.
results. Before drug administration, a transition from light to dark reduced both choroidal hemodynamic parameters by 11% to 20%. Neither phenylephrine nor placebo altered basal choroidal blood flow or choroidal blood flow responses to the light/dark transitions. By contrast, the NOS inhibitor L-NMMA significantly reduced basal choroidal blood flow by 20.5% ± 5.9% (P < 0.001) and basal fundus pulsation amplitude by 21.5% ± 4.8% (P < 0.001). In addition, the response of subfoveal choroidal blood flow (–6.2% ± 3.2%; P = 0.008) and fundus pulsation amplitude (–4.2% ± 2.4%; P < 0.001) to the light/dark transition was significantly diminished.
conclusions. The present study indicates that NO plays a role in the choroidal blood flow decrease during a transition from light to dark. Given that L-NMMA is a nonspecific inhibitor of NOS, the present study does not clarify whether this NO is from endothelial or neural sources.
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