Table 1.

Date	Article	Author	Category	Description
1983	Pathophysiology of ischemic cell death: I. Time of onset of irreversible damage; importance of the different components of the ischemic insult.	Ames A, Nesbett FB	Pathological	Studies the effect of various lengths of ischemia on rabbit retinas in vitro in order to pinpoint the onset of cell death. Results showed that after 20 minutes of ischemia, the retina cells could recover but after 30 minutes there was extensive irreversible damage.
1983	Pathophysiology of ischemic cell death: II. Changes in plasma membrane permeability and cell volume.	Ames A 3rd, Nesbett FB	Pathological	Studies the effect of changes in cell volume on cell death related to ischemic insult using rabbit retinas in vitro. Results show that cell swelling correlated closely with loss of viability as evidenced by failure to reinstitute protein synthesis, but the swelling appeared to be the consequence rather than the cause of the initial irreversible damage.
1983	Pathophysiology of ischemic cell death: III. Role of extracellular factors.	Ames A 3rd, Nesbett FB	Pathological	Studies the effect of extracellular changes that occur during ischemia on cell survival through deprivation of O2 and substrate of rabbit retina cells in vitro. Results demonstrate that recovery is significantly effected by changes in the extracellular fluid resulting from ischemia.
1990	Effect of the calcium antagonist, nifedipine, on ischemic retinal dysfunction.	Crosson CE et al	Pathological	Hypothesizes that retinal degeneration associated with ischemia may result from accumulation of calcium intracellularly. The hypothesis is supported after rats treated with calcium channel agonists were shown to have protection against ischemic damage in the retina.
1991	Accumulation of amino acids and hydroxyl free radicals in brain and retina of gerbil after transient ischemia.	Delbarre G et al	Pathological	Examines the levels of amino acids and hydroxyl free radicals in gerbil cerebral ischemia through examination of the occular fundus. The ischemic group in comparison to control shows increased levels of aspartate, glutamate, GABA, and 2,5 DHBA.
1992	Open-channel block of N-methyl-D- aspartate (NMDA) responses by memantine: therapeutic advantage against NMDA receptor-mediated neurotoxicity.	Chen HS et al	Therapeutic	Studies the effect of memantine, an adamantane derivative, on channels activated by NMDA receptor stimulation. The article shows that the drug blocks these channels, contributing to a therapeutic effect against neurotoxicity in the animal model, but unlike other similar drugs it is well tolerated clinically, suggesting future clinical uses.
1995	Effect of Daflon 500 mg, a flavonoid drug, on neurological signs, levels of free radicals and electroretinogram in the gerbil after ischemia-reperfusion injury.	Delbarre B et al	Therapeutic	Studies the effects of Daflon 500 mg, a flavanoid drug, on ischemia-reperfusion injury. Concludes that the drug could interact with hydroxyl free radicals, which have a deleterious effect in ischemic tissues, particularly in the retina.
1995	Effect of piribedil, a D-2 dopaminergic agonist, on dopamine, amino acids, and free radicals in gerbil brain after cerebral ischemia.	Delbarre B et al	Therapeutic	Tests the action of D-2 agonist piribedil on gerbil brains after ischemia reprefusion/insult in order to observe if it inhibits release of excitatory amino acids implicated in cerebral ischemia. Finds that piribedil presents a neuroprotective effect and reverses the increase of dopamine, exitatory amino acids, and hydroxyl-free radicals after ischemia reperfusion/insult.
1996	Taurine in gerbil retina: changes during ischemia reperfusion/insult (I.R.I.) and aging.	Delbarre B et al	Pathological	Examines levels of taurine in gerbil retinas in animals effected by ischemia and control animals at a variety of ages. The study finds that animals from the ischemic group regularly increase taurine levels in the retina throughout the course of their aging while animals from the control group have low levels of taurine at early ages, the levels reach a plateau, and then decrease with age.
1997	Intravitreal injection of ganglioside GM1 after ischemia reduces retinal damage in rats.	Mohand-Said S et al	Therapeutic	Evaluates the protective effect of GM1 administered intravitreally after ischemia on retinal lesions. Concludes that GM1 given intravitreally successfully protects the rat retina from pressure-induced ischemic injury and that this protection could be of therapeutic interest.
1998	Tacrolimus (FK506) attenuates leukocyte accumulation after transient retinal ischemia.	Tsujikawa A et al	Pathological	Evaluates quantitatively the inhibitory effects of tacrolimus on leukocyte rolling and on subsequent leukocyte accumulation in vivo after transient retinal ischemia and the protective effects of tacrolimus on ischemia- induced neural damage. Successfully demonstrates this inhibitory effect and provides quantitative analysis on the results.
1998	Acetylsalicylate administered during simulated ischemia reduces the recovery of neuronal function in the in vitro rabbit retina.	Maynard KI et al	Mechanistic	Studies whether the effects of aspirin on ischemia are due to it acting directly on the CNS or through some other method. Concludes that lysine acetylsalicylate inhibits CNS neurotransmission, but not phototransduction, in a concentration- dependent manner.
2000	Chronic cerebral hypoperfusion: loss of pupillary reflex, visual impairment and retinal neurodegeneration.	Davidson CM et al	Pathological	Studies the effects of chronic cerebral ischemia on vision and retina by performing permanent bilateral occlusions of common cartoid arteries on adult rats. Procedure causes loss of pupillary reflex and degeneration of photoreceptors and retinal ganglion cells in a number of rats.
2002	Retinal and optic nerve degeneration after chronic carotid ligation: time course and role of light exposure.	Stephens WD et al	Pathological	Examines the effects of chronic retinal ischemia in an animal model involving permanent carotid occlusion. Finds that ischemic damage to the optic nerve causes loss of pupillary reflex and death of retinal ganglion cells in a subset of rats.
2003	Argatroban attenuates leukocyte- and platelet-endothelial cell interactions after transient retinal ischemia.	Miyahara S et al	Pathological	The study attempts to evaluate quantitatively the inhibitory effects of the thrombin inhibitor argatroban on leukocyte- and platelet-endothelial cell interactions after transient retinal ischemia. It finds that argatroban treatment successfully suppresses leukocyte- and platelet-endothelial cell interactions after transient retinal ischemia.
2003	Functional and cellular responses in a novel rodent model of anterior ischemic optic neuropathy.	Bernstein SL et al	Pathological	Study creates a new rodent model for anterior ischemic optic neuropathy (AION). Accomplishes a photoembolic stroke model that is directly analogous to human AION through use of histologic, electrophysiological, molecular-, and cell biological methods.
2003	Non-erythroid functions of erythropoietin.	Gassmann M et al	Pathological	Discusses roles of EPO outside of Erythropoesis, showing the expression of EPO and its receptor in the brain, spinal cord, retina, and testis. Discusses the future of applications for EPO in a clinical setting.
2004	Retinal ischemia: mechanisms of damage and potential therapeutic strategies.	Osborne NN et al	Therapeutic	Discusses the myriad of emerging treatments that are generating success in diminishing the negative effects of retinal ischemia in animal models, and how translating these treatments to clinical models is proving difficult.
2004	Effect of erythropoietin axotomy- induced apoptosis in rat retinal ganglion cells.	Weishaupt JH et al	Mechanistic	Examines EPO signal transduction in vivo and the usefulness of EPO in the prevention of the chronic, purely apoptotic neuronal cell death that contributes to vision loss in glaucoma and the progression of neurodegenerative diseases. Concludes based on results that EPO has potential as a therapeudic molecule against apoptotic neuronal cell death.
2004	Science review: recombinant human erythropoietin in critical illness: a role beyond anemia?	Coleman T et al	Pathological	Discusses the potential utility of EPO as a protective cytokine in the context of acute critical illness and suggests parameters for a proof-of-concept clinical study.
2005	Erythropoietin protects from axotomy-induced degeneration of retinal ganglion cells by activating ERK-1/-2.	Kilic U et al	Therapeutic	Examines the effect of Erythropoietin on the degeneration of retinal ganglion cells in transgenic mouse line tg21. The results reveal that the retinal ganglion cells of Epo transgenic tg21 mice were protected against degenaration in comparison to the wild-type control group.