Oxygen and blood flow: players in the pathogenesis of glaucoma
Oxygen and blood flow: players in the pathogenesis of glaucoma
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发表时间：
2008-01
期刊：
影响因子：
2.2
通讯作者：
M. Mozaffarieh;M. Grieshaber;J. Flammer
中科院分区：
文献类型：
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作者：
M. Mozaffarieh;M. Grieshaber;J. Flammer
目的 POAG 中 IOP 的增加是由于房水通过小梁网 (TM) 流出的阻力增加。方法 导致 TM 相应变化的确切机制尚不清楚。然而我们知道，所有动脉硬化的危险因素也是眼压升高的危险因素。结果 眼压升高与这些因素之间的关联相对较弱，但仍然显着。与动脉硬化的发病机制类似，氧化应激在 TM 损伤的发生过程中发挥着重要作用。结论 对于青光眼性视神经病变（GON）的发病机制知之甚少。显然，动脉硬化的危险因素通过增加眼压发挥作用。然而，当校正眼压后，这些因素仅起次要作用。相反，与自身调节紊乱相关的因素，特别是全身性原发性血管失调 (PVD)，会增加 GON 的风险。这在正常眼压性青光眼患者中最容易观察到。自动调节不足会增加眼灌注不稳定的机会，从而增加氧气供应不稳定的机会。这反过来又会导致氧化应激。视神经乳头轴突内的超氧化物 (O2-) 浓度增加。如果邻近的星形胶质细胞被机械或缺血应激激活，过量产生的一氧化氮 (NO) 分子也会扩散到轴突中并与氧气融合。产生的过氧硝酸盐 (ONOO-) 在轴突内向视网膜和外侧膝状核扩散并诱导细胞凋亡。
Purpose The increase of IOP in POAG is due an increased resistance of aqueous outflow through the trabecular meshwork (TM). Methods The exact mechanisms leading to the corresponding changes in the TM are not yet known. We know, however, that all risk factors for arteriosclerosis are also risk factors for an increase in IOP. Results The association between IOP increase and these factors is relatively weak but nevertheless significant. Similar to the pathogenesis of arteriosclerosis, oxidative stress plays a role in the development of TM damage. Conclusions Even less is known about the pathogenesis of glaucomatous optic neuropathy (GON). Obviously the risk factors for arteriosclerosis play a role via increasing the IOP. When corrected for IOP, however, these factors only play a minor role. In contrast, factors associated with disturbed autoregulation, in particular a systemic primary vascular dysregulation (PVD), increase the risk for GON. This is best observed in normal tension glaucoma patients. An insufficient autoregulation increases the chance for an unstable ocular perfusion and thereby an unstable oxygen supply. This, in turn, leads to oxidative stress. The concentration of superoxide (O2-) within the axons of the optic nerve head increases. If neighboring astrocytes are activated, either by mechanical or by ischemic stress, in excess produced nitric oxide (NO) molecules diffuse also into the axons and fuse with oxygen. The resulting peroxynitrat (ONOO-) diffuses within the axons towards the retina and the lateral geniculate nucleus and induces apoptosis.