February 1994
Volume 35, Issue 2
Free
Articles  |   February 1994
Intraretinal study of cat electroretinogram during retinal ischemia-reperfusion with extracellular K+ concentration microelectrodes.
Author Affiliations
  • K Hiroi
    Department of Ophthalmology, Kyoto University Faculty of Medicine, Japan.
  • F Yamamoto
    Department of Ophthalmology, Kyoto University Faculty of Medicine, Japan.
  • Y Honda
    Department of Ophthalmology, Kyoto University Faculty of Medicine, Japan.
Investigative Ophthalmology & Visual Science February 1994, Vol.35, 656-663. doi:
  • Views
  • PDF
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      K Hiroi, F Yamamoto, Y Honda; Intraretinal study of cat electroretinogram during retinal ischemia-reperfusion with extracellular K+ concentration microelectrodes.. Invest. Ophthalmol. Vis. Sci. 1994;35(2):656-663.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

PURPOSE: Intraretinal electroretinograms (ERG) during retinal ischemia-reperfusion were analyzed to clarify which cells are affected in the cat dark-adapted eye. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×