Changes in pO2 induce retinal autoregulation in vitro.

Vascular autoregulation maintains stable retinal function in vivo in the face of changes in arterial pO2. We observed autoregulatory changes in the flow of perfusate through the isolated cat eye in response to changes in pO2. Hydrostatic perfusion pressure and all other variables of the perfusate, except for pO2, were kept constant. Throughout the experiments the viability of the eye was monitored by electroretinography. In nine short periods of hypoxia, pO2 of the perfusate was reduced by 12%-42% compared to the control. In eight of these experiments the flow rate of the perfusate increased significantly. Retinal vasodilation during hypoxia was also documented by indocyanine green angiography, monitored by TV, and photographed. In seven periods of hyperoxia, pO2 was raised by 7%-38%. In all cases the flow of the perfusate decreased. These changes in flow are interpreted as resulting from autoregulative vasodilation and vasoconstriction of the retinal vessels. The b-wave of the ERG increased and decreased parallel with pO2 of the perfusate. This indicates that autoregulation in vitro does not sufficiently compensate for changes in pO2. This is in contrast to our findings from a previous study in the anesthetized cat.