Hiroi K, Yamamoto F, Honda Y
Department of Ophthalmology, Kyoto University Faculty of Medicine, Japan.
Invest Ophthalmol Vis Sci. 1994 Feb;35(2):656-63.
Intraretinal electroretinograms (ERG) during retinal ischemia-reperfusion were analyzed to clarify which cells are affected in the cat dark-adapted eye.
Ischemia was induced by raising the intraocular pressure above arterial systolic pressure in vivo. Double-barreled microelectrodes were used to record the intraretinal ERGs and the light-evoked [K+]o decrease in the subretinal space. Vitreal ERGs, the standing potential and the transepithelial resistance were also recorded.
After 10 minutes of ischemia, vitreal ERG b- and c-waves had recovered fully in 2 hours, and after 30 minutes of ischemia, recovered approximately 85% and 77% of their control amplitudes in 4 hours, respectively. At the early period of reperfusion after 10 minutes of ischemia we observed the supernormal c-wave (124% of its control amplitude, n = 10) with an elevated standing potential. The transepithelial potential (TEP) c-wave increased without changes of slow PIII and transepithelial resistance when the supernormal amplitudes occurred. The light-evoked [K+]o decrease in the subretinal space (90% retinal depth) in the area centralis recovered to about 90% of the control amplitude in 2 hours, and after 30 minutes of ischemia recovered to about 70% of the control amplitudes in 4 hours. The recovery courses of the slow PIII and TEP c-wave were almost the same as that of the light-evoked [K+]o decrease.
The temporary supernormal amplitude of the ERG c-wave was originated from the retinal pigment epithelium (RPE) during the early period of reperfusion after 10 minutes of ischemia. The photoreceptors, Muller cell and RPE are responsible for the changes in the light-evoked [K+]o decrease, a slow PIII and TEP c-wave, respectively. Intraretinal recordings suggested that after ischemia of 10 to 30 minutes duration, the responses of photoreceptors, Muller cells and the RPE recovered with a similar time course. These findings suggest that in all cases, primarily photoreceptors were damaged.
分析视网膜缺血再灌注期间的视网膜内视网膜电图（ERG），以明确在猫暗适应眼中哪些细胞受到影响。
通过在体内将眼压升高至动脉收缩压以上来诱导缺血。使用双管微电极记录视网膜内ERG以及视网膜下间隙中光诱发的[K+]o降低。还记录了玻璃体ERG、静息电位和跨上皮电阻。
缺血10分钟后，玻璃体ERG的b波和c波在2小时内完全恢复，缺血30分钟后，在4小时内分别恢复到其对照振幅的约85%和77%。在缺血10分钟后的再灌注早期，我们观察到超常c波（其对照振幅的124%，n = 10），静息电位升高。当出现超常振幅时，跨上皮电位（TEP）c波增加，而慢PIII和跨上皮电阻无变化。中央凹区域视网膜下间隙（视网膜深度的90%）中光诱发的[K+]o降低在2小时内恢复到对照振幅的约90%，缺血30分钟后在4小时内恢复到对照振幅的约70%。慢PIII和TEP c波的恢复过程与光诱发的[K+]o降低的恢复过程几乎相同。
ERG c波的暂时超常振幅起源于缺血10分钟后再灌注早期的视网膜色素上皮（RPE）。光感受器、穆勒细胞和RPE分别负责光诱发的[K+]o降低、慢PIII和TEP c波的变化。视网膜内记录表明，在持续10至30分钟的缺血后，光感受器、穆勒细胞和RPE的反应以相似的时间进程恢复。这些发现表明，在所有情况下，主要是光感受器受到了损伤。
