Abstract
In the retina, blood flow and neural activity are tightly coupled. Stimulation of the retina with flickering light is accompanied by an increase in blood flow. The current study seeks to investigate whether an increase in oxygen tension modulates flicker (FL)-induced vasodilatation in the human retina. A total of 52 healthy volunteers were included. Via a breathing mask, 100% oxygen (O2) was administered in one, a mixture of 8% carbon dioxide and 92% oxygen (C/O) in a second cohort. Retinal vessel diameters were measured with a Vessel Analyzer and FL responses were assessed before and during the breathing periods. At baseline, FL stimulation increased retinal vessel diameters by +3.7±2.3% in arteries and by +5.1±3.7% in veins. Breathing of C/O led to a decrease in arterial (−9.0±6.9%) and venous (−11.3±5.9%) vessel calibers. Flicker response was increased to 5.7±2.5% in arteries and to 8.6±4.1% in veins. Breathing of pure O2 induced a vasoconstriction of vessel diameters by −14.0±5.3% in arteries and −18.4±7.0% in veins and increased FL responses in arteries (+6.2±2.8%) and veins (+7.2±3.1%). Systemic hyperoxia increases FL-induced retinal vasodilatation in the retina. The mechanism by which oxygen modulates the hyperemic response to FL stimulation remains to be elucidated.
Highlights
Functional hyperemia, first described for the brain more than 100 years ago,[1] is an important physiologic mechanism that allows for the adaptation of blood flow to changed metabolic demands of the tissue.[2]
Systemic blood pressure was slightly higher in the O2 group than in the carbon dioxide and 92% oxygen (C/O) group, all other BL parameters were comparable between groups
To the best of our knowledge, this is the first study providing evidence that oxygen has a modulatory effect in FLinduced retinal vasodilatation in humans. This is in contrast to animal studies where systemic hyperoxia did not affect neurovascular coupling in the brain[15] or the retina.[11]
Summary
Functional hyperemia, first described for the brain more than 100 years ago,[1] is an important physiologic mechanism that allows for the adaptation of blood flow to changed metabolic demands of the tissue.[2] As for the eye, it has been shown that an increase in retinal and optic nerve head blood flow can be evoked by stimulation with flickering light.[3,4] The current view is that visual stimulation leads to augmented neural activity, which in turn increases the metabolic needs of the tissue and subsequently triggers the increase in blood flow.[5] This functional hyperemic response, termed as neuro-vascular coupling, is considered necessary for proper retinal function assuring sufficient supply with oxygen and nutrients.[2,6] As such, it has been shown that several ocular diseases such as glaucoma[7] or diabetic retinopathy[8,9] are associated with impaired vasodilatation in response to flicker (FL) stimulation. Whether increased oxygen delivery may alter neuro-vascular coupling in the human retina has never been tested experimentally
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