Neuroretinal function during systemic hyperoxia and hypercapnia in humans.

Abstract

Breathing pure oxygen (O2) or carbogen is known to have differential effects on the retinal and choroidal blood flow. Our objective was to evaluate the effects these hemodynamic changes have on various retinal neurons receiving their vital nutrients from these two vascular beds. To that effect, we recorded the photopic flash electroretinogram (fERG) and oscillatory potentials (OP's) in man. Eighteen adults participated in two test sessions to examine the effects of breathing pure O2 or carbogen on the fERG's and OP's. The retinal potentials were recorded at the end of each of the following breathing phases: (1) room air for 5 min, (2) pure O2 or carbogen for 5 min, (3) immediately after the flow of gas was stopped, and (4) 10 min after the flow of gas was stopped. The heart rate, respiratory rate, oxygen saturation (Sao2), and end-tidal carbon dioxide (Etco2) were monitored. The blood pressure and intraocular pressure were measured to derive the ocular perfusion pressure. Breathing pure O2 increased Sao2, decreased heart rate and Etco2, but did not alter respiratory rate and ocular perfusion pressure. Breathing carbogen increased Sao2, Etco2, and ocular perfusion pressure, decreased respiratory rate but did not alter heart rate. The fERG's and OP's were not detrimentally affected by breathing either pure oxygen or carbogen. Only OP4 was delayed at the end of testing in the O2 session. Our results show that the neural generators of the photopic fERG's and OP's in man are largely unaltered by the degree of systemic hyperoxia and hypercapnia induced and their reported effects on retinal and choroidal hemodynamics. These results, combined with earlier studies showing that some components of the scotopic fERG's and OP's were altered during similar testing conditions, suggest that the photopic system is more resistant than the scotopic system to altered ocular hemodynamics.