Transretinal pO2 profiles were recorded during normoxia and hyperoxia in normal and ischemic retinal regions in anesthetized miniature pigs, using double-barrelled recess-type microelectrodes. In normoxia and hyperoxia, pO2 in the normal region decreased from the inner retina and the choroid toward the midretina, indicating that the choroid cannot supply O2 to the entire normal retina. Preretinal and transretinal pO2 measurements in ischemic regions following laser occlusion of a retinal branch vein showed that in normoxia the direction of pO2 gradients prevents O2 diffusing from the choroid to reach the inner retina. This explains why the ischemic regions remain hypoxic. On the contrary, during hyperoxia the intraretinal pO2 gradient indicates an O2 flux from the choroid to the inner retina, resulting in a marked increase in preretinal pO2 in the affected regions. Hence hyperoxia could be a useful tool for restoring the oxygen supply to the inner, hypoxic retinal layers; unfortunately it cannot be used in clinical practice. Parabulbar injections of dexamethasone induce a transitory increase in preretinal pO2, probably by reducing the outer retinal consumption of O2 and thus allowing O2 which diffuses through the choroid to reach and restore the inner retinal hypoxia; clinical experience has shown that parabulbar dexamethasone injections may be effective in the treatment of venous branch occlusion.