The effect of interruption of the short posterior ciliary arteries on slow axoplasmic transport and histology within the optic nerve of the rhesus monkey.

Tritiated leucine was injected into the vitreous of rhesus monkey eyes to make it available for protein synthesis by the ganglion cells. The short posterior ciliary arteries were cut three hours later or several weeks prior to the leucine injection. A reduction of labeled protein within the retrolaminar optic nerve was seen in all eyes so treated. Autoradiography revealed a diffuse reduction of axoplasmic transport into these optic nerve heads. There was consistent evidence of focal obstruction of labeled protein at the interface between the lamina scleralis and retrolaminar optic nerve. Vacuoles appeared in the most severely affected areas. These histologic changes were followed by gliosis in the areas of ischemic damage. Glaucomatous cupping of the optic nerve head was not seen within six weeks following the induced ischemia.