Animal Models of Retinal Ischemia
نویسنده
چکیده
Retinal ischemia is a frequent source of irreparable visual impairment and even loss of sight, affecting over a hundred million individuals in the world. It is associated with a wide range of clinical retinal disorders, like ischemic optic neuropathies, obstructive retinopathies, carotid occlusive disorders, diabetic retinopathy and glaucoma. Retinal ischemia occurs when the blood supply to retina is inadequate to meet the metabolic requirements of the retina. If treatment is not given to fix this imbalance, the outcome is irreversible, ischemic and apoptotic cascades resulting in cell death. Appropriate study models, particularly animal models, are necessary for further understanding the etiology, pathology, and evolution of retinal ischemia and also in order to help in the evaluation, development, and improvement of therapeutic strategies. Accordingly, quite a few in-vivo and ex-vivo mammalian models have been developed to study this syndrome. The rat models of retinal ischemia are frequently used, because the distribution of retinal and choroidal blood supply is quite similar to that in humans. The retina has been extensively used for the study of pathophysiology of ischemia and mechanism of damage triggered by ischemia and excitotoxicity. Compared to all the other tissues, retina has a higher metabolic rate; any disturbance in blood supply can have an effect on the supply of oxygen and the substrates leading to retinal ischemia. The retina has a dual blood supply. The photoreceptors and most of the outer plexiform layer (OPL) are nourished by choriocapillaries, while the inner retinal layers are nourished by the central retinal artery. The actual effects of retinal ischemia vary, depending on the position of the occlusion. It is clear that occlusion of the retinal artery leads to inner retinal ischemia only, but occlusion of ophthalmic artery leads to global retinal ischemia, as it supplies blood to the central retinal artery as well as choriocapillaries.
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تاریخ انتشار 2017