A rat model of chronic pressure-induced optic nerve damage

John Morrison, C. G. Moore, Lisa M H Deppmeier, Bruce G. Gold, Charles K. Meshul, Elaine Johnson

Research output: Contribution to journalArticle

397 Citations (Scopus)

Abstract

To develop unilateral, chronically elevated intraocular pressure in rats, episcleral veins were injected with hypertonic saline and the intraocular pressure was monitored with a Tono-Pen XL tonometer. Histologic analyses of eyes with differing degrees and durations of intraocular pressure elevation were performed to ascertain the effects of these pressures on the optic nerve. Out of 20 consecutive animals, nine had elevations of intraocular pressure following a single injection, while subsequent injections raised intraocular pressure in seven others. One eye became hypotonous. In the remaining animals, subsequent injections sufficient to raise intraocular pressure were deliberately withheld, to determine the possible direct effects of injections on the optic nerve. Mean sustained pressure elevations ranged from 7 to 28 mm Hg and the retinal vasculature remained perfused in all eyes. Optic nerve cross sections from eyes without intraocular pressure elevation appeared identical to those from uninjected eyes, while nerves from eyes with the greatest intraocular pressure rise demonstrated axonal damage that involved 100% of the neural area. Eyes with either less severe pressure elevations or shorter durations showed partial damage, ranging from 0.5% to 10.4% of the neural area. In 70% of these nerves, damage was concentrated in the superior temporal region. Within the optic nerve head, often associated with astrocytes, axons contained abnormal accumulations of membrane-bound vesicles and mitochondria. The anterior chamber angles showed sclerosis of the trabecular meshwork with anterior synechiae, but Schlemm's canal, collector channels and aqueous veins appeared patent. Unilateral sclerosis of the trabecular meshwork produces sustained elevation of intraocular pressure in rats with optic nerve damage that in many ways resembles that seen in human glaucoma. Understanding the mechanism of nerve damage in this model may provide new insights into the pathogenesis of human glaucoma.

Original languageEnglish (US)
Pages (from-to)85-96
Number of pages12
JournalExperimental Eye Research
Volume64
Issue number1
DOIs
StatePublished - Jan 1997

Fingerprint

Optic Nerve
Intraocular Pressure
Pressure
Trabecular Meshwork
Injections
Sclerosis
Glaucoma
Veins
Esotropia
Optic Disk
Anterior Chamber
Temporal Lobe
Astrocytes
Axons
Mitochondria
Membranes

Keywords

  • Glaucoma
  • Glaucomatous optic neuropathy
  • Intraocular pressure
  • Rat model
  • Tonometry

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems

Cite this

A rat model of chronic pressure-induced optic nerve damage. / Morrison, John; Moore, C. G.; Deppmeier, Lisa M H; Gold, Bruce G.; Meshul, Charles K.; Johnson, Elaine.

In: Experimental Eye Research, Vol. 64, No. 1, 01.1997, p. 85-96.

Research output: Contribution to journalArticle

Morrison, John ; Moore, C. G. ; Deppmeier, Lisa M H ; Gold, Bruce G. ; Meshul, Charles K. ; Johnson, Elaine. / A rat model of chronic pressure-induced optic nerve damage. In: Experimental Eye Research. 1997 ; Vol. 64, No. 1. pp. 85-96.
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