Neuroprotective effects of brief ischemia pulses in an experimental model glaucoma

BELFORTE, NA; SANDE, PH; DE ZAVALÍA NURIA; FERNANDEZ, DC; SILBERMAN, D.M; CHIANELLI, MS; ROSENSTEIN, RE

Huerta Grande, Córdoba

Congreso; XXVI Congreso Anual de la Sociedad Argentina de Investigación en Neurociencias; 2011

Sociedad Argentina de Investigación en Neurociencias

Glaucoma is a leading cause of acquired blindness which may involve an ischemic-like insult to retinal ganglion cells and optic nerve head (ONH). We investigated the effect of a weekly application of brief ischemia pulses (ischemic conditioning) on the 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: intraocular pressure (IOP), retinal and visual pathway function (electroretinogram (ERG), and visual evoked potentials (VEPs)) and histology of the retina and ONH. Retinal thiobarbituric acid substances levels were assessed as an index of lipid peroxidation. Ischemic conditioning significantly preserved ERG, VEPs, retinal and ONH structure from glaucomatous damage, without changes in IOP. Moreover, ischemia pulses abrogated the increase in lipid peroxidation induced by CS. These results suggest that induction of ischemic tolerance could constitute a new therapeutic strategy in glaucoma treatment.