To evaluate the effects of chronic optic nerve ischemia in a nonhumanprimate model and to evaluate the regional variability of axonal loss.
Unilateral ischemic optic neuropathy was induced by administration ofendothelin-1 to the retrobulbar space via osmotic pumps in 12 primates for6 to 12 months. The transversely cut sections were stained and divided into16 regions. Average axonal density in each region was quantified and comparedwith the untreated contralateral control eyes.
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 onoverall 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 inthe damaged nerves; the damaged regions often clustered within specific quadrants.
Chronic ischemia induced by local administration of endothelin-1 causessignificant loss of optic nerve axons with varying regional susceptibility.
Localized damage occurs in other types of optic neuropathy, such asglaucoma, and may result from regional differences in anatomy, metabolism,or vasculature of the primate optic nerve.