Physiology of retinal oxygenation

Abstract

SummaryThe retina receives O2 from retinal and choroidal circulations. Both vascular beds can now be imaged with noninvasive spectrophotometric oximetry in human subjects. This allows study of normal O2 metabolism and physiology and clinical research in retinal disease. Normal physiology: Technical and biological variability in retinal O2 saturation is low compared to most clinical parameters. Test‐retest studies show standard deviations of about 1% and in a healthy population the standard deviation is only 5–11% of the mean, low compared for example to IOP measurements. Retinal O2 saturation is relatively stable with age and shows only a minor reduction over decades of life. Retinal oximetry reliably detects retinal O2 saturation consumption due to changes in illumination. Retinal and choroidal oximetry data agree well with invasive studies in animals and human subjects. Ischemic retinopathies: Abnormal O2 saturation has been documented in diabetic retinopathy, retinal vein and artery occlusions and neovascular AMD. This agrees well with invasive PO2 studies and presence of Hypoxia‐Inducible‐Factor in these diseases. Atrophic retinopathies: Retinal atrophy in glaucoma and retinitis pigmentosa reduces O2 consumption and this is detected by retinal oximetry. Retinal oximetry may be a good method to quantify progressive retinal atrophy.