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Aim-The eVect of breathing 100% oxygen on retinal and optic nerve head capillary blood flow in smokers and non-smokers was investigated using scanning laser Doppler flowmetry (SLDF) as a new noninvasive method to visualise and quantify ocular blood flow. Method-10 eyes of 10 young healthy nonsmoking volunteers (mean age 26 (SD 3) years) and nine eyes of nine young healthy smoking volunteers (mean age 26 (4) years) were investigated. All participants were asked not to smoke or consume caVeine containing drinks for at least 4 hours before the measurements. Blood flow measurements were performed before and after 100% oxygen was applied to the subjects through a mask over a period of 5 minutes (6 litres per minute). Juxtapapillary retinal and optic nerve head blood flow were determined in arbitrary units using SLDF representing a combination of laser Doppler flowmetry and a scanning laser system allowing visualisation and quantification of the retinal and optic nerve head blood flow. Blood flow was determined in an area of 100 µm × 100 µm. The level of carboxyhaemoglobin was determined in all subjects. A Wilcoxon matched pairs signed ranks test (nonparametric) was used for statistical evaluation. Results-In the non-smoking group, retinal 'flow' was reduced by 33% (p = 0.005), optic nerve head 'flow' by 37% (p = 0.005). In the smoking group retinal flow was reduced by 10% (p = 0.01), optic nerve head flow by 13% (p <0.008). The diVerence in reactivity to oxygen breathing between smokers and non-smokers was highly significant (p <0.00001). Increased carboxyhaemoglobin levels were not found in either of the groups. A significant reduction of the mean arterial blood pressure of 6% (5%) (p <0.02) was observed in the non-smoking group after administration of oxygen. Conclusion-These results indicate that hyperoxia leads to a decrease in capillary blood flow of the retina and optic nerve head secondary to vasoconstriction, and that smokers do not respond to oxygen breathing as non-smokers do. The findings might be based on factors such as long term eVects of nicotine on the sympathetic and parasympathetic nervous system. (Br J Ophthalmol 1997;81:365-369)

The blood flow in the uvea in cats and monkeys during acute increases of arterial blood pressure is well controlied by a sympathetic mechanism protecting the eye from overperfusion. Ocular macrocirculation (ophthalmic artery) and ocular microcirculation (iris) were examined in 22 healthy subjects during acute increases of arterial blood pressure induced by physical exercise (125 W). With a data aquisition and storage software in real time mode several parameters of ocular perfusion and systemic functions were measured simultaneously. Blood flow parameters were measured in the ophthalmic artery by pulsed Doppler sonography and in the iris by laser Doppler flowmetry. Systolic, diastolic, and mean velocities of the ophthalmic artery peak velocity pulse curve, the ophthalmic artery mean velocity pulse curve, and the iris velocity pulse curve were estimated off line. The ophthalmic artery mean velocity pulse curve resembles the integrated velocity of ali erythrocytes in the vessel including the slowly running celis near the vessel wail. The iris velocity pulse curve was calculated by a special statistic procedure (ALDF). After exercise there was a significant increase in systolic and diastolic blood pressure and heart rate. The pulse curve of the ophthalmic artery showed significantly increased systolic and decreased diastolic velocities. The vascular resistance of the branches of the ophthalmic artery increased significantly. The iridal vasculature showed no significant change in blood celi velocity but an increased vascular resistance.It was observed that the elevated perfusion pressure was associated with an increased vascular resistance and a constant mean blood velocity in the ophthalmic artery and iridal vessels. The paraliel elevation of vascular resistance and blood pressure during exercise may be the reason for a constant blood flow in the ophthalmic artery and the iris. This may be accounted for by a sympathetic mechanism for protecting the eye from overperfusion. (BrJ3 Ophthalmol 1994; 78: 461-465) Several authors observed in rabbits, cats, and monkeys, a good regulation of the ocular blood flow during increased perfusion pressures. In these observations sympathetic stimulation reduced the blood flow in all parts of the uvea in these animals. The