September 1996
Volume 37, Issue 10
Free
Articles  |   September 1996
Retinal ganglion cell death after different transient periods of pressure-induced ischemia and survival intervals. A quantitative in vivo study.
Author Affiliations
  • I Sellés-Navarro
    Laboratorio de Oftalmología Experimental, Facultad de Medicina, Universidad de Murcia, Madrid, Spain.
  • M P Villegas-Pérez
    Laboratorio de Oftalmología Experimental, Facultad de Medicina, Universidad de Murcia, Madrid, Spain.
  • M Salvador-Silva
    Laboratorio de Oftalmología Experimental, Facultad de Medicina, Universidad de Murcia, Madrid, Spain.
  • J M Ruiz-Gómez
    Laboratorio de Oftalmología Experimental, Facultad de Medicina, Universidad de Murcia, Madrid, Spain.
  • M Vidal-Sanz
    Laboratorio de Oftalmología Experimental, Facultad de Medicina, Universidad de Murcia, Madrid, Spain.
Investigative Ophthalmology & Visual Science September 1996, Vol.37, 2002-2014. doi:
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    • Get Citation

      I Sellés-Navarro, M P Villegas-Pérez, M Salvador-Silva, J M Ruiz-Gómez, M Vidal-Sanz; Retinal ganglion cell death after different transient periods of pressure-induced ischemia and survival intervals. A quantitative in vivo study.. Invest. Ophthalmol. Vis. Sci. 1996;37(10):2002-2014.

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Abstract

PURPOSE: To quantitate in vivo retinal ganglion cell (RGC) survival after transient periods of pressure-induced ischemia of the rat retina and after different survival intervals. METHODS: In adult rats, RGCs were labeled with fluorogold applied to their main targets in the brain. Seven days later, in several groups of rats, the left retinas were subjected to transient periods of ischemia of 30, 45, 60, 75, 90, 105, or 120 minutes, respectively, by increasing the intraocular pressure (IOP) of the left eye above systolic values. Five, 7, 14, and 30 days later, the rats were killed, and their retinas were prepared as wholemounts for examination under fluorescence microscopy to estimate RGC survival. RESULTS: The authors found that periods of ischemia of 30 and 45 minutes do not induce RGC death; longer periods of transient ischemia induce the death of a proportion of RGCs, and the proportion increases with the duration of the ischemia; RGC death, which can be observed as early as 5 days after ischemia, continues during the 30-day study period; and periods of ischemia that last 90 minutes or more cause the death of approximately 95% of the RGC population 30 days later. CONCLUSIONS: Increases of the IOP above systolic levels for periods of 60 minutes or more result in RGC loss in the rat retina. Both the duration of the initial transient period of ischemia and the duration of the survival period influence the proportion of RGC death.

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