Abstract
Glaucoma is a leading cause of acquired blindness which may involve an ischemic-like insult to retinal ganglion cells and optic nerve head. We investigated the effect of a weekly application of brief ischemia pulses (ischemic conditioning) on the rat retinal damage induced by experimental glaucoma. Glaucoma was induced by weekly injections of chondroitin sulfate (CS) in the rat eye anterior chamber. Retinal ischemia was induced by increasing intraocular pressure to 120 mmHg for 5 min; this maneuver started after 6 weekly injections of vehicle or CS and was weekly repeated in one eye, while the contralateral eye was submitted to a sham procedure. Glaucoma was evaluated in terms of: i) intraocular pressure (IOP), ii) retinal function (electroretinogram (ERG)), iii) visual pathway function (visual evoked potentials, (VEPs)) iv) histology of the retina and optic nerve head. Retinal thiobarbituric acid substances levels were assessed as an index of lipid peroxidation. Ischemic conditioning significantly preserved ERG, VEPs, as well as retinal and optic nerve head structure from glaucomatous damage, without changes in IOP. Moreover, ischemia pulses abrogated the increase in lipid peroxidation induced by experimental glaucoma. These results indicate that induction of ischemic tolerance could constitute a fertile avenue for the development of new therapeutic strategies in glaucoma treatment.
Highlights
Glaucoma is a leading cause of blindness worldwide, characterized by specific visual field defects due to the loss of retinal ganglion cells (RGCs) and damage to the optic nerve head (ONH)
The present results indicate that a weekly application of 5-min retinal ischemia pulses which showed no effect per se, abrogated functional and histological alterations induced by chronic ocular hypertension
The retinal protection induced by ischemia pulses was independent from ocular hypertension, as shown by the fact that ischemia pulses did not affect the increase in intraocular pressure (IOP) induced by chondrotin sulfate (CS) injections
Summary
Glaucoma is a leading cause of blindness worldwide, characterized by specific visual field defects due to the loss of retinal ganglion cells (RGCs) and damage to the optic nerve head (ONH). We have developed a model of glaucoma in rats through weekly injections of chondrotin sulfate (CS) in the eye anterior chamber. Injections of CS for 6 or 10 (but not 3) weeks significantly decrease the electroretinographic activity as well as flash visual evoked potentials (VEPs). After 10 weeks of ocular hypertension induced by CS, a significant loss of ganglion cell layer (GCL) cells and optic nerve fibers occurs in eyes treated with
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
