May 2007
Volume 48, Issue 13
ARVO Annual Meeting Abstract  |   May 2007
Characteristics of Modeling Pressure-Induced Optic Nerve Damage in Elderly Rat Eyes
Author Affiliations & Notes
  • J. C. Morrison
    Dept of Ophthalmology, Casey Eye Institute-OHSU, Portland, Oregon
  • W. O. Cepurna
    Dept of Ophthalmology, Casey Eye Institute-OHSU, Portland, Oregon
  • L. Jia
    Dept of Ophthalmology, Casey Eye Institute-OHSU, Portland, Oregon
  • E. C. Johnson
    Dept of Ophthalmology, Casey Eye Institute-OHSU, Portland, Oregon
  • Footnotes
    Commercial Relationships J.C. Morrison, Alcon Laboratories, F; W.O. Cepurna, None; L. Jia, None; E.C. Johnson, None.
  • Footnotes
    Support NIH Grant EY10145 and EY16866
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 3662. doi:
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      J. C. Morrison, W. O. Cepurna, L. Jia, E. C. Johnson; Characteristics of Modeling Pressure-Induced Optic Nerve Damage in Elderly Rat Eyes. Invest. Ophthalmol. Vis. Sci. 2007;48(13):3662.

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

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Purpose:: Age is a well-recognized risk factor for glaucoma. Models of pressure-induced optic nerve damage in elderly eyes are essential for developing neuroprotective strategies in this apparently vulnerable population. This report describes factors necessary to produce appropriate elevations of IOP in elderly rat eyes and compares the pressure-susceptibility of their optic nerves to those of younger adult animals.

Methods:: 137 elderly Brown Norway rats (age 28 months) were used. Hypertonic saline was injected via episcleral veins into the limbal vasculature, using a plastic ring around the equator to direct saline to the limbus and produce scarring of the aqueous humor outflow pathways. Animals were then monitored and awake IOP measured by Tonopen 4 days per week. After 5 weeks, animals were sacrificed and the optic nerves sectioned and graded for injury on a previously established scale of 1 (no degeneration) to 5 (degeneration involving the entire nerve). A separate group of 8 month-old (adult) animals underwent similar procedures to produce similar pressures and allow comparison of optic nerve susceptibility to IOP with elderly animals.

Results:: A protocol well established for 8 month old animals produced mean IOP elevations > 40 mm Hg in 37 out of 79 elderly animals (46%). All but one of these had injury grades of 4.5 or higher. This marked pressure response may be due to narrowing of the angle from increased thickness of the aged lens and a greater degree of angle closure following saline injection. Subsequent injections in an additional 58 animals using a ring modified to restrict saline exposure to half of the angle circumference resulted in mean IOP > 40 in only 4 animals (7%). Compared to 8 month-old animals, moderate pressures (cumulative IOP 40 to 200 mm Hg-days) in elderly eyes produced a significantly greater degree of optic nerve damage (2-way ANOVA, p<0.05). This difference was not apparent in eyes with higher pressures and extensive optic nerve damage. Sickness and unintended death preventing adequate assessment of optic nerve damage occurred in 24 elderly animals, either prior to or following injection.

Conclusions:: Special handling and modifications of experimental procedures established in younger animals are needed to produce mild pressure rises in fragile, elderly rats. With this, it is possible to demonstrate that the elderly optic nerve is more sensitive to experimentally elevated IOP than younger adults. Differences in gene response to elevated IOP in both the retina and optic nerve head may underlie this increased susceptibility to IOP.

Keywords: optic nerve • aging • intraocular pressure 

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