This Article  • Full text  • PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Citing articles on ISI (11)  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Topic Collections  • Neurology  • Neuro-ophthalmology  • Glaucoma  • Alert me on articles by topic  Social Bookmarking   What's this?

George A. Cioffi, MD; Lin Wang, PhD; Brad Fortune, PhD; Grant Cull, B Ag Sci; Jin Dong, PhD; Bang Bui, PhD; E. Michael Van Buskirk, MD

Arch Ophthalmol. 2004;122:1517-1525.

Objectives  To evaluate the effects of chronic optic nerve ischemia in a nonhuman primate model and to evaluate the regional variability of axonal loss.

Methods  Unilateral ischemic optic neuropathy was induced by administration of endothelin-1 to the retrobulbar space via osmotic pumps in 12 primates for 6 to 12 months. The transversely cut sections were stained and divided into 16 regions. Average axonal density in each region was quantified and compared with the untreated contralateral control eyes.

Results  Mean axonal density was 208 310/mm² and 220 661/mm² in treated and control eyes, respectively (P = .03, 1-tailed paired t test), for the entire group. Two-way analysis of variance showed a significant effect of endothelin-1 on overall axonal density for the experimental group (P<.001). Among the nerves with significant axonal loss, the mean axonal loss was 11.6% (4%-21%). Regional mapping of the damage showed the axonal loss varied in the damaged nerves; the damaged regions often clustered within specific quadrants.

Conclusion  Chronic ischemia induced by local administration of endothelin-1 causes significant loss of optic nerve axons with varying regional susceptibility.

Clinical Relevance  Localized damage occurs in other types of optic neuropathy, such as glaucoma, and may result from regional differences in anatomy, metabolism, or vasculature of the primate optic nerve.

From the Discoveries in Sight, Devers Eye Institute, Portland, Ore. The authors have no relevant financial interest in this article.

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Longitudinal profile of retinal ganglion cell damage assessed with blue-light confocal scanning laser ophthalmoscopy after ischaemic reperfusion injury
Leung et al.
Br. J. Ophthalmol. 2009;93:964-968.
ABSTRACT | FULL TEXT  

Acute Endothelin-1 Application Induces Reversible Fast Axonal Transport Blockade in Adult Rat Optic Nerve
Wang et al.
IOVS 2008;49:961-967.
ABSTRACT | FULL TEXT  

Blood flow in glaucoma
Orgul
Br. J. Ophthalmol. 2007;91:3-5.
FULL TEXT  

Endothelin B receptor in human glaucoma and experimentally induced optic nerve damage.
Wang et al.
Arch Ophthalmol 2006;124:717-724.
ABSTRACT | FULL TEXT  

Anterior Optic Nerve Capillary Blood Flow Response to Diurnal Variation of Mean Ocular Perfusion Pressure in Early Untreated Primary Open-Angle Glaucoma
Sehi et al.
IOVS 2005;46:4581-4587.
ABSTRACT | FULL TEXT  

Endothelin-1 Enhances Glutamate-Induced Retinal Cell Death, Possibly through ETA Receptors
Kobayashi et al.
IOVS 2005;46:4684-4690.
ABSTRACT | FULL TEXT