Background: To investigate the effects of microvascular compromise on the expression of oxidative proteins in the\r\noptic nerve head.\r\nMethods: Endothelin-1 (0.1 �µg/day) was delivered to the perineural region of the anterior optic nerve by\r\nosmotically driven minipumps for two, four, and eight weeks in ten rabbits, respectively. As a control, a balanced\r\nsalt solution was delivered for two and eight weeks in five rabbits, respectively. Expression of oxyproteins in the\r\ncornea, vitreous, retina, and optic nerve head for each time period was determined using the OxyBlot protein\r\noxidation detection kit. Retina was stained with H&E and TUNEL for histological examination.\r\nResults: There was a significant increase in the expression of oxyproteins in the optic nerve head after two weeks\r\nof endothelin-1 administration (p < 0.001, Mann Whitney U test). In contrast, there was no expression of oxyproteins\r\nin the cornea, retina, or vitreous. The number of cells in the retinal ganglion cell layer, inner nuclear layer, and outer\r\nnuclear layer decreased remarkably with time in the endothelin-1-treated group. Furthermore, the inner and outer\r\nnuclear layers, as well as the inner and outer plexiform layers, became thinner over time.\r\nConclusions: Administration of endothelin-1 to the microvasculature of the optic nerve leads to increased\r\nexpression of oxyproteins in the optic nerve head and loss of retinal ganglion cells.
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