[Experimental branch vein occlusion: the effect of carbogen breathing on preretinal PO2]

To evaluate the variations in preretinal PO2 in normal and in ischemic postexperimental branch vein occlusion (BRVO) retinal areas during normoxia, hyperoxia (100% O2) and carbogen (95% O2, 5% CO2) breathing.

Preretinal PO2 measurements were obtained in intervascular retinal areas far from the retinal vessels of 13 anesthetized miniature pigs with oxygen-sensitive microelectrodes (10 microm tip diameter) introduced through the vitreous cavity by a micromanipulator. The microelectrode tip was placed at 50 microm from the vitreoretinal interface in the preretinal vitreous. PO2 was measured continuously for 10 minutes in systemic normoxia, hyperoxia (100% O2 breathing) and carbogen (95% O2, 5% CO2) breathing. A BRVO was induced with an argon green laser, and oxygen measurements were repeated in normoxia, hyperoxia and carbogen breathing.

In hyperoxia, preretinal PO2 remained almost constant in both normal retinas (DeltaPO2=1.33 mmHg +/- 3.39; n=13) and ischemic retinas (DeltaPO2=3.73 mmHg +/- 2.84; n=8), although systemic PaO2 significantly increased. Carbogen breathing induced a significant increase in systemic PaO2 and PaCO2. Furthermore, it significantly increased preretinal PO2: DeltaPO2=23.05 mmHg +/- 17.06 (n=12) in normal retinas, and DeltaPO2=22.54 mmHg +/- 5.96 (n=6) in ischemic retinal areas.

Systemic hyperoxia does not increase preretinal PO2 significantly in normal and ischemic post-BRVO retinal areas of miniature pigs, as hyperoxia induces a decrease in the retinal blood flow. Carbogen breathing significantly increases preretinal PO2 in normal and in ischemic post-BRVO retinal areas. This effect is probably due to the vasodilatation of the retinal arterioles induced by the intravascular PaCO2 increase.