To date, calculated measurements of DO
2 have not been reported in humans. Since DO
2 is the product of TRBF and arterial oxygen content, TRBF alone provides only partial information about oxygen delivery to the retina. Similarly, MO
2 is the product of TRBF and arteriovenous O
2 difference,
17 thus measuring either SO
2 or TRBF individually would likely lead to incorrect conclusions with regard to MO
2. Alternatively, MO
2 can be expressed as the product of DO
2 and the inner retinal oxygen extraction fraction (OEF).
18,19 OEF quantifies how much of the oxygen available from the retinal vasculature is extracted by the retinal tissue for metabolism. Under physiologic or pathologic challenges, compensatory changes in DO
2 and OEF respond in order to maintain MO
2. Conversely, alterations in MO
2 can play a role in regulating DO
2. In healthy subjects, MO
2 was measured under normoxia and hyperoxia.
20,21 Furthermore, MO
2 was shown to be reduced in subjects with diabetic retinopathy.
22,23 However, MO
2 has not been evaluated in sickle cell retinopathy (SCR), in which vision-threatening retinal capillary occlusions, nonperfusion, ischemia, and neovascularization are known to occur.
24–32 The purpose of the current study was to establish measurements of DO
2 and MO
2 in healthy subjects and test the hypothesis that DO
2 and MO
2 are reduced in SCR subjects.