Pathophysiobgical Study of Retinal Ischenia-with Ion-seledive Microelectrode

我们研究了视网膜缺血再灌注过程中的电生理变化。记录视网膜电图（ERG）、微电极视网膜电图（ERG）及视网膜内离子浓度变化。通过升高眼压诱导视网膜缺血，观察再灌注过程中电位的变化。缺血10 ~ 30min后的ERG b波和c波在再灌注6h后逐渐恢复。缺血30分钟后未见完全恢复。为探讨自由基在再灌注损伤中的作用，静脉给予自由基清除剂超氧化物歧化酶和过氧化氢酶。两种药物均未显示ERG的显著改善，但在早期观察到c波明显恢复。视网膜内记录显示与ERG相似的恢复。光感受器和视网膜色素上皮也受到损伤。再灌注后数小时，光诱发的光感受器外碱化减少，提示光感受器代谢减少。该空间中光诱发[K+]变化的减少表明光感受器的离子通道或泵功能降低。

We studied the electrophysiological change of the retina during ischemia-reperfusion in vivo cat. The electroretinogram (ERG), intraretinal ERG with microelectrodes and the change of ion concentration in the retina were recorded. In order to observe the change in potentials during reperfusion, retinal ischemia was induced by raising intraocular pressure. The ERG b- and c-wave after 10-30 minutes of ischemia were gradually recovered in 6 hours of reperfusion. After 30 minutes of ischemia complete recovery was not observed. To investigate the role of free radicals in reperfusion injury, superoxide dismutase and catalase, which were free radical scavengers, were given intravenously. Both agents did not show the significant improvement of ERG, although during early period the remarkable recovery of c-wave was observed. The intraretinal recordings showed similar recovery to the ERG.The photoreceptors and retinal pigment epithelium vere also damaged. The fact that the light-evoked alkalinizaton outside photoreceptors was reduced few hous after reperfusion suggests the reduction of photoreceptor's metabolism. The decrease of light-evoked [K+] change in that space suggests that the ion channel or pump function of photoreceptors is reduced.