Nakazaki S, Nao-i N, Sawada A
Department of Ophthalmology, Miyazaki Medical College, Japan.
Curr Eye Res. 1998 Apr;17(4):384-91. doi: 10.1080/02713689808951219.
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 determine the mechanisms involved in the recovery of the RPE during the post-hypoxic period.
In vitro preparations of chick retina-RPE-choroid were studied by potassium-selective microelectrodes placed in the subretinal space. In addition, single-barrel microelectrodes were used to obtain intracellular recordings from the RPE cells. The perfusate was bubbled continuously with 95% oxygen and 5% carbon dioxide for the control condition and replaced by 95% nitrogen and 5% carbon dioxide to induce hypoxia.
Hypoxia induced a significant reduction 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-tissue 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-hypoxic period. The c-wave amplitude was temporarily elevated (263.7 +/- 77.4% of pre-hypoxic control) because of the enhanced trans-epithelial c-wave and without a light-evoked decrease in subretinal [K+]o.
The trans-tissue potential and the c-wave were markedly decreased during hypoxia. During the post-hypoxic period, both potential recovered with transient supernormalities in two phases. The results suggested that the hypoxic changes resulted directly from changes of the RPE membranes and indirectly from a change in the subretinal [K+]o but were not mediated by the light-evoked decrease in subretinal [K+]o.
确定雏鸡视网膜色素上皮(RPE)电位缺氧诱导改变及RPE光诱发反应所涉及的细胞机制。此外,确定缺氧后时期RPE恢复所涉及的机制。
通过置于视网膜下间隙的钾选择性微电极研究雏鸡视网膜-RPE-脉络膜的体外标本。此外,使用单管微电极从RPE细胞获得细胞内记录。在对照条件下,灌注液持续用95%氧气和5%二氧化碳鼓泡,并用95%氮气和5%二氧化碳替代以诱导缺氧。
缺氧导致跨组织电位显著降低,发现这是由RPE顶端膜去极化引起的。这种去极化是由视网膜下[K+]o升高诱导的。缺氧期间c波也明显降低或消失。缺氧后恢复有两个阶段:最初跨组织电位因基底膜去极化而有小幅增加,随后是顶端膜超极化。在此缺氧后时期,跨组织电位和c波在两个阶段也表现为超常。由于跨上皮c波增强且视网膜下[K+]o无光照诱发降低,c波振幅暂时升高(缺氧前对照的263.7±77.4%)。
缺氧期间跨组织电位和c波明显降低。在缺氧后时期,两种电位均在两个阶段出现短暂超常后恢复。结果表明,缺氧变化直接源于RPE膜的改变,间接源于视网膜下[K+]o的变化,但不是由视网膜下[K+]o的光照诱发降低介导的。