缺血性视神经病变:疾病机制的模型。

S V Potarazu
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引用次数: 0

摘要

前路缺血性视神经病变(AION)是一种累及视盘头梗死的疾病。与动脉病变有关的因素已被很好地理解,但对更常见的非动脉病变知之甚少。更好地了解血压和眼压之间的变化可以提供更多关于视神经头本身循环的信息。此外,视神经头的自我调节作用(或缺乏)以及血管内皮介导因子的作用可能在该疾病中发挥重要作用。在细胞水平上,缺血引起的轴突损伤似乎是由突然的离子转移介导的。在这个过程中一个重要的信使是钠介导的钙转运体,它促进钙离子的流入,导致蛋白水解酶的激活,最终导致轴突死亡。因此存在多种治疗选择,通过阻断钙通道或抑制转运蛋白来防止进一步的轴突损伤。
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Ischemic optic neuropathy: models for mechanism of disease.

Anterior ischemic optic neuropathy (AION) is an entity which involves infarction of the optic disc head. Factors involved with the arteritic variety are well understood, but less is known about the more common nonarteritic variety. A better understanding of variations between blood pressure and intraocular pressure could provide more information about circulation to the optic nerve head itself. Furthermore, the role of autoregulation at the optic nerve head (or lack of) as well as the role of vascular endothelium-mediated factors could play a large role in the disease. At a cellular level, axonal damage from ischemia appears to be mediated by sudden ionic shifts. A significant messenger in this process is a sodium-mediated calcium transporter which facilitates the influx of calcium ions leading to activation of proteolytic enzymes and ultimately axonal death. Various treatment options thus exist by either blocking calcium channels or inhibiting the transporter in order to prevent further axonal damage.

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