Electrophysiological consequences of retinal hypoxia.

Experiments on cats show that electrical activity of the inner (proximal) retina is unaffected during systemic hypoxia as long as arterial oxygen tension (PaO2) is above 40 mm Hg. This is due to effective regulation of inner retinal tissue PO2 by the retinal circulation. In contrast, some electrical signals generated in the outer (distal) retina begin to change when PaO2 falls below 70-80 mmHg. The outer retinal responses are generated by the retinal pigment epithelium, but their susceptibility to hypoxia results primarily from their dependence on photoreceptors. Photoreceptor metabolism is sensitive to hypoxia because of the high oxygen consumption of photoreceptors and their reliance on the choroidal circulation, which cannot regulate PO2 in the outer retina. Retinal electrophysiology and oxygen distribution are altered by acutely elevated intraocular pressure just as by hypoxia. These results raise the question as to how inner retinal function can be preserved when outer retinal function is altered. The explanations proposed relate to (1) differences in conditions of light adaptation in different studies, (2) the possible inappropriateness of the previous measurements in the inner retina for revealing photoreceptor dysfunction, and (3) a possible preservation of photoreceptor electrical responses when their metabolism is altered. Comparison of cat and human studies suggests that the human retina is affected in much the same way during hypoxia as the cat retina, but further experiments are required for an understanding of the role of hypoxia in human disease.