A new experimental model of glaucoma in rats through intracameral injections of hyaluronic acid.

Abstract

An experimental model of pressure-induced optic nerve damage would greatly facilitate the understanding of the cellular events leading to ganglion cell death, and how they are influenced by intraocular pressure and other risk factors associated to glaucoma. The aim of the present report was to study the effect of a long-term increase of intraocular pressure in rats induced by intracameral injections of hyaluronic acid with respect to electroretinographic activity and retinal and optic nerve histology. For this purpose, hyaluronic acid was injected weekly in the rat anterior chamber of one eye, whereas the contralateral eye was injected with saline solution. The results showed a significant decrease of oscillatory potentials and a- and b-wave amplitude of the scotopic electroretinogram after 3 or 6 weeks of hyaluronic acid administration, respectively. These parameters were further reduced after 10 weeks of treatment with hyaluronic acid. No significant changes in anterior chamber angle structures from hyaluronic acid- and vehicle-injected eyes were observed, whereas a significant loss of ganglion cell layer cells and of optic nerve axons were detected in animals that received hyaluronic acid for 10 weeks, as compared to eyes injected with saline solution. In summary, present results indicate that the chronic administration of hyaluronic acid induced a significant decrease in the electroretinographic activity and histological changes in the retina and optic nerve that seem consistent with some features of chronic open-angle glaucoma. Therefore, this could be an experimental model to study the cellular mechanisms by which elevated intraocular pressure damages the optic nerve and the retina.