Flicker light stimulation increases the diameters of retinal arterioles and venules. The relative increase of 5.6% and 7.6% for the CRAEs and CRVEs, respectively, found in this study is in good agreement with findings from measurements in single vessels.
25 –27 Because, by the Hagen-Poiseuille law, the flow is proportional to the fourth power of the vessel diameter, this increase indicates an augmentation of the retinal blood flow by approximately 20%. At least in part, this increase might be necessary to fulfill the elevated metabolic demand of the inner retina during neuronal activity. Measurements by Robert Linsenmeier (personal communication, 2009) revealed a slight decrease of retinal PO
2 during neuronal activity evoked by flicker light. This drop of oxygen concentration may trigger vasodilation to maintain sufficient supply to the tissue. Because the oxygen consumption by the tissue might be higher during activation, a higher diffusion rate from the vessel to the tissue is needed. As diffusion is driven by the concentration gradient, an increased intravascular PO
2 is the consequence of metabolic activity. This may explain the increase in venous SO
2, which is linked to the PO
2 by the hemoglobin oxygen binding curve, found in this study. Similar results were found in rats measuring the PO
2 by an oxygen-quenchable phosphorescent porphyrin probe.
28,29 During flicker, the arterial PO
2 increased, whereas the venous PO
2 remained constant, indicating an augmented oxygen supply. In our experiments, we may have an arterial PO
2 increase too, which is not observable with the measurement of hemoglobin SO
2, which cannot exceed 100%. The constant venous PO
2 readings in previous rat experiments conflict with our results; however, in these experiments, venous PO
2 was unphysiologically low because of the anesthetics used.
28 Under these conditions, blood flow may have been increased to its maximum but failed to meet the metabolic needs of the tissue.