Abstract
Background/aims The relative effects of simultaneously administered oxygen and carbon dioxide on vascular resistance are unknown. The purpose of the study was to investigate the independent effect of oxygen partial pressure on hypercarbia-induced vasodilation in the retinal arterioles. Methods Twelve young healthy volunteers participated in the study. End-tidal partial pressure of carbon dioxide was raised 23% from the baseline (i.e. air) at normoxia and then maintained constant while end-tidal partial pressure of oxygen (P etO 2) was raised in a stepwise incremental fashion. Retinal vessel diameter and blood velocity were measured in the superior-temporal arteriole using the Canon Laser Blood Flowmeter. Results Hypercarbia resulted in a 16% increase in blood velocity and a 22% increase in blood flow ( p < 0.05). At maximal hyperoxia (group mean P etO 2 of 556 mm Hg) vessel diameter, blood velocity and flow were reduced by 9%, 22% and 36%, respectively, relative to baseline ( p < 0.001). Conclusion The concentration-dependent vasoconstrictive effect of oxygen in retinal arterioles was quantified for the first time by implementing precise control of end-tidal concentrations of CO 2 and O 2. Oxygen-induced vasoconstriction is sufficiently potent to offset and reverse hypercarbia-induced vasodilation.
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