Although the influence of duration and frequency of ischemia pulses on retinal protection deserves to be further examined, these results indicate that a significant restoration of retinal alterations provoked by chronic ocular hypertension can be achieved by the procedure performed herein. Evidence has progressively accumulated to suggest that vascular insufficiency plays an important role in the pathogenesis of glaucomatous neuropathy, and a strong case has been made out to support the view that glaucoma may involve an ischemic-like insult to RGCs. IPC and PostC are highly effective strategies to protect the retina from an acute and deleterious ischemic episode. The precise AP24534 Src-bcr-Abl inhibitor mechanisms responsible for the retinal protection against glaucomatous damage induced by ischemia pulses remain to be established. Several common mechanisms have been involved in glaucomatous and ischemic damage. Oxidative stress, excitotoxicity, cell acidosis, inflammation, and others mechanisms acting in tandem are of considerable importance in both retinal ischemia and glaucoma. Among all retinal neurons, RGCs are most susceptible to ischemic and glaucomatous damage. Several lines of evidence support that oxidative damage plays a major role in glaucoma pathogenesis. In that sense, we have demonstrated that ocular hypertension provokes a significant decrease in the retinal endogenous antioxidant defense system activity. Moreover, retinal lipid peroxidation significantly increases in a time-of-hypertension-dependent manner. The present results indicate that ocular hypertension induced by chronic injections of CS significantly increased retinal lipid peroxidation, and that induction of ischemic tolerance decreased this parameter. Thus, without excluding the activation of other transduction pathways associated with retinal IPC, such as adenosine, KATP channels, Protein Kinase C, heat shock proteins and NO among others, and based on the fact that ischemia pulses abrogated the increase in lipid peroxidation, it is tempting to speculate that the induction of ischemic conditioning could behave as an antioxidant therapy. Brief ischemia or hypoxia serve as prototypical conditioning stimuli; however, ischemic tolerance can be induced by exposing animals or cells to diverse type of endogenous or exogenous stimuli that are not necessarily hypoxic or ischemic in nature, such as hyperbaric oxygenation, or hyperthermia among others. Recently, we have shown that a moderate inflammation induced by a single intravitreal injection of bacterial lipopolysaccharide provides retinal protection against ischemia/reperfusion injury. In fact, IPC also induces retinal protection against a nonischemic insult, such as light-induced injury. It has been postulated that ischemic tolerance provokes the attenuation of broad categories of injury-inducing mechanisms, including excitotoxicity, ion/pH imbalance, oxidative and nitrosative stress, metabolic dysfunction, inflammation and, ultimately, necrotic and apoptotic cell death. Several of these mechanisms have been involved in glaucomatous damage. Thus, although the present results do not necessarily support the involvement of retinal ischemia in glaucoma.