EFFECTS OF HYPOXIA AND POSTHYPOXIC RECOVERY ON CHICK RETINAL-PIGMENT EPITHELIUM POTENTIALS AND LIGHT-EVOKED RESPONSES IN-VITRO

Purpose. To determine the cellular mechanisms involved in the hypoxia- induced alteration of the retinal pigment epithelium (RPE) potentials and the light-evoked responses of the RPE in chicks. In addition, to d etermine the mechanisms involved in the recovery of the RPE during the post-hypoxic period. Methods. In vitro preparations of chick retina-R PE-choroid were studied by potassium-selective microelectrodes placed in the subretinal space. In addition, single-barrel microelectrodes we re used to obtain intracellular recordings from the RPE cells. The per fusate was bubbled continuously with 95% oxygen and 5% carbon dioxide for the control condition and replaced by 95% nitrogen and 5% carbon d ioxide to induce hypoxia. Results. Hypoxia induced a significant reduc tion of the trans-tissue potential which was found to result from the depolarization of the apical membrane of the RPE. This depolarization was induced by an increase of subretinal [K+](o). The c-wave was also markedly decreased or abolished during hypoxia, There were two phases of post-hypoxic recovery: an initial small increase in the trans-tissu e potential resulting from a basal membrane depolarization followed by an apical membrane hyperpolarization. The trans-tissue potential and the c-wave also were supernormal in two phases during this post-hypoxi c period. The c-wave amplitude was temporarily elevated (263.7 +/- 77. 4% of pn-hypoxic control) because of the enhanced transepithelial c-wa ve and without a light-evoked decrease in subretinal [K+](o). Conclusi ons. The trans-tissue potential and the c-wave were markedly decreased during hypoxia. During the post-hypoxic period, both potential recove red with transient supernormalities in two phases. The results suggest ed that the hypoxic changes resulted directly from changes of the RPE membranes and indirectly from a change in the subretinal [K+](o) but w ere not mediated by the light-evoked decrease in subretinal [K+](o).