Introductory comments on blood flow autoregulation in the optic nerve head and vascular risk factors in glaucoma

Introductory comments on blood flow autoregulation in the optic nerve head and vascular risk factors in glaucoma
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DOI:
10.1016/s0039-6257(99)00046-6
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发表时间:
1999-06-01
影响因子:
5.1
通讯作者:
Anderson, DR
Anderson, DR
中科院分区:
医学2区
文献类型:
--
作者:
Anderson, DR

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广泛怀疑组织缺血引发或参与青光眼的视盘损伤。细节没有很好地描述。特别令人困惑的是,青光眼和前部缺血性视神经病变的临床表现是明确分开的,前部缺血性视神经病变也是一种假定的缺血性疾病。当眼出口点的静脉压因眼内压(IOP)升高时,动静脉压差降低。只有通过血流自动调节才能维持营养。如果个体的自动调节功能受损,则可能导致眼内压诱导的缺血,这可能是由于先天性缺陷,也可能是由于血管痉挛性疾病。如果另一种疾病(例如,动脉粥样硬化)已经导致许多自动调节能力被利用,使得很少或没有留下对IOP的额外挑战的响应。缺血也可能是由于血小板或凝血异常导致的微血管闭塞,可能诱发不依赖于IOP的青光眼性视神经病变。需要更好地理解致病机制(以及它在各种情况下可能如何不同),以更成功地预测个体的青光眼损伤风险,做出关于治疗积极性的决定,并且有一天,除了降低IOP之外或代替降低IOP,针对存在的血管异常类型进行指导治疗。(C)1999年,Elsevier Science Inc. All rights reserved.
It is widely suspected that tissue ischemia initiates or participates in optic disk damage in glaucoma. The details are not well delineated. Particularly puzzling is the clear separation of the clinical appearances of glaucoma and anterior ischemic optic neuropathy, which is also a presumed ischemic disease. When venous pressure at the exit point from the eye is elevated by intraocular pressure (IOP), the arteriovenous pressure difference is reduced. Nutrition is maintained only because of blood flow autoregulation. Intraocular pressure-induced ischemia can result if autoregulation is impaired in an individual, either because of an innate deficiency or, perhaps, as a result of vasospastic disease. Autoregulation can also be impaired if another disease (e.g., an atheroma) has caused much of the autoregulatory capacity to be already utilized, so that little or none is left to respond to the additional challenge of IOP. Ischemia might also result from microvascular occlusion with platelet or clotting abnormalities, perhaps inducing glaucomatous optic neuropathy that is not dependent on IOP. A better understanding of, the pathogenic mechanism (and how it may be different in various cases) is needed to predict more successfully an individual's risk of glaucomatous damage, to make decisions about the aggressiveness of treatment, and, one day, to direct therapy at the type of vascular abnormality present, in addition to or instead of lowering IOP. (C) 1999 by Elsevier Science Inc. All rights reserved.