Table 1.
Summary of experimental models of OIS.
| Publication | Strain | Method | Main Outcome |
|---|---|---|---|
| Leahy et al., 2020 [16] | Long–Evans rats | BCCAO | Abnormal changes in artery/vein diameter, vein velocity, total retinal blood flow, and oxygen delivery and metabolism |
| Huang et al., 2014 [17] | Clean-grade Wister rats | BCCAO | Longer artery filling time; decreases in ocular blood flow (the pupil, iris, and total eye) |
| Qin et al., 2019 [18] | Sprague–Dawley rats | BCCAO | Decreases in amplitudes of scotopic a-wave and b-wave; decreases in retinal thickness; disorder and damage in retinal ganglion cells (especially karyopyknosis, chromatic agglutination, and decreased or swelling organelles); disorder and damage in photoreceptor cells |
| Sivilia et al., 2009 [19] | Sprague–Dawley rats | BCCAO | PLR loss; decreases in the outer plexiform layer and the inner plexiform and ganglion cell layers without affecting the outer nuclear and inner nuclear layers |
| Lavinsky et al., 2006 [20] | Wistar rats | BCCAO | PLR loss; more impairment in retinal thickness and ganglion cell density in BCCAO-operated rats with PLR loss |
| Davidson et al., 2000 [21] | Sprague–Dawley rats | BCCAO | PLR loss; general retinal damage and visual loss |
| Yamamoto et al., 2006 [22] | Wistar rats | BCCAO | Molecular alterations in various pro- and antiapoptotic factors and retinal cell markers such as cleaved caspase-3, ubiquitin, COX-2, HSP70, calbindin, BRN3, microtubule-associated protein 2, and synaptophysin |
| Chidlow et al., 2014 [23] | Sprague–Dawley rats | BCCAO | Increases in HSP27 protein expression in the retina and optic nerve (especially, in the ganglion cell and inner plexiform layers) |
| Chidlow et al., 2010 [24] | Sprague–Dawley rats | BCCAO | Gradual increases in HSP27 and αB-crystallin expressions and gradual decreases in NFL and β3-tubulin protein expressions found in the proximal optic nerve; deposition of extracellular matrix components (collagen I, collagen VI, and laminin) |
| Wang et al., 2016 [25] | Hypertensive and normotensive Wistar–Kyoto rats | BCCAO | Higher dysfunction rates in the PLR under hypertension; extensive avascular areas of blood vessels; dramatic decreases in retinal thickness |
| Holman et al., 2010 [26] | Sprague–Dawley rats with streptozotocin | BCCAO | Retinal protection (such as preservation of retinal thickness and survival of BRN3-, Islet-1-, PGP 9.5-, and calbindin-positive retinal cells); pathological gliosis (such as activation of astrocytes, Müller cells, and microglia) reduction by short-term hyperglycemia |
| Crespo-Garcia et al., 2018 [27] | C57BL/6J mice | BCCAO/BCCAS | Retinal vein dilatation; mobilization and accumulation of mononuclear phagocytes in surrounding veins; decreases in amplitudes in scotopic a-wave, b-wave, and oscillatory potentials; synaptic degeneration (vesicular glutamate transporter 1, C-terminal-binding protein 2, protein kinase C-α, and calbindin-D28k) |
| Lee et al., 2019 [28] | C57BL/6 mice | UCCAO | Retinal HIF-2α stabilization; increases in Epo mRNA expression; decreases in total retinal thickness |
| Lee and Kang et al., 2020 [29] | C57BL/6 mice | UCCAO | Abnormal retinal blood perfusion; eyelid drooping; retinal HIF-1α stabilization; acute GFAP-positive gliosis; chronic retinal thinning |
| Lee and Jeong et al., 2021 [30] | C57BL/6 mice | UCCAO | Decreases in amplitudes of scotopic b-wave; chronic retinal gliosis; transient retinal cell death |
| Lee et al., 2021 [31] | C57BL/6 mice | UCCAO | No change in PLR or IOP; acute reversible cataract development; visual evoked potential reduction; NeuN-positive cell loss; chronic retinal inflammation |
| Ling et al., 2017 [32] | C57BL/6 mice | BICAO | Abnormal ocular blood flow; alterations in retinal thickness |
| Ogishima et al., 2011 [33] | ddY mice | Occlusion of the PPA and ECA | Decreases in ocular blood flow; functional and histologic damage in the inner retina |