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Susanne Dallinger, Guido T. Dorner, Roland Wenzel, Ursula Graselli, Oliver Findl, Hans-Georg Eichler, Michael Wolzt, Leopold Schmetterer; Endothelin-1 Contributes to Hyperoxia-Induced Vasoconstriction in the Human Retina. Invest. Ophthalmol. Vis. Sci. 2000;41(3):864-869.
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purpose. There is evidence that ocular blood flow strongly depends on arterial
oxygen tension. Results from recent animal studies indicate that the
vasoconstrictor response to hyperoxia may be mediated in part by an
increased production of endothelin (ET)-1. In an effort to answer the
question whether the retinal vasoconstrictive response to hyperoxia in
humans is mediated through ET-1, changes in ocular hemodynamics induced
by 100% O2 breathing were studied in the absence and
presence of an ETA receptor antagonist (BQ-123).
methods. The study was a randomized, placebo-controlled, double-masked,
balanced, three-way crossover design. On separate study days 15 healthy
male subjects received infusions of BQ-123 (either 60 μg/min or 120μ
g/min) or placebo. The effects of BQ-123 or placebo on
hyperoxia-induced (100% O2 breathing) changes in retinal
and pulsatile choroidal blood flow were assessed with the blue-field
entoptic technique and with laser interferometric measurement of fundus
results. During baseline conditions, hyperoxia caused a decrease in retinal
blood flow between −29% and −34% (P < 0.001)
and a decrease in fundus pulsation amplitude between −7% and −8%
(P < 0.001). BQ-123 dose dependently blunted the
response to hyperoxia in the retina (60 μg/min: −25%, 120 μg/min:−
20%; P = 0.003), but not in the choroid.
conclusions. These results indicate that ET-1 contributes to hyperoxia-induced
retinal vasoconstriction in the human retina.
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