Flicker Light-Induced Vasodilatation in the Human Retina: Effect of Lactate and Changes in Mean Arterial Pressure

PURPOSE. Diffuse luminance flicker light increases retinal and optic nerve head blood flow in animals and humans, but the exact mechanisms that mediate increased flow have yet to be identified. In the current study, the effect of increased plasma lactate levels on flicker-induced vasodilatation in the retina was investigated in three independent studies in healthy humans. METHODS. In the first study, plasma lactate concentrations were increased by bicycle exercise in 12 volunteers, and the change in retinal vessel diameter to 8-Hz square-wave flicker stimulation was measured with the Zeiss Retinal Vessel Analyzer (Carl Zeiss Meditec, Oberkochen, Germany). In a different study, sodium lactate was administered intravenously, and flicker responses were measured in 12 subjects. As a control experiment accounting for pressure increases induced by exercise, the effect of elevated ocular perfusion pressure on the flicker response was investigated during tyramine infusion (n = 12). RESULTS. The increase in plasma lactate concentration during intravenous infusion from 1.3 ± 0.4 to 6.3 mmol/L and during dynamic exercise from 1.2 ± 0.3 to 9.4 mmol/L decreased flicker responses in retinal arteries from 5.3% ± 0.9% to 1.7% ± 0.6% (P < 0.001) and from 3.6% ± 0.6% to 2.0% ± 0.8% (P = 0.03), respectively. In contrast, an increase of mean blood pressure from 81 ± 3 to 92 ± 3 mm Hg after tyramine infusion had no significant effect on flicker-induced vasodilatation in retinal arteries and veins. CONCLUSIONS. The signaling between neuronal activity and flow response in the human retina is sensitive to changes in blood lactate levels, whereas changes in systemic blood pressure have no major effect. Whether an increased cytosolic redox impairment contributes to flicker-induced vasodilatation has yet to be clarified.