Harris A, Jonescu-Cuypers C, Martin B, Kagemann L, Zalish M, Garzozi H J
Department of Ophthalmology, Indiana University School of Medicine, Indianapolis, IN 46202-5175, USA.
Acta Ophthalmol Scand. 2001 Aug;79(4):336-41. doi: 10.1034/j.1600-0420.2001.079004336.x.
Factors other than intraocular pressure (IOP) elevation must be involved in initiation and progression of glaucoma. An additional element in disease causation may be ischemia in the retina and optic nerve head. Ischemic damage to neurons in the CNS is similar mechanistically and histopathologically to changes seen in glaucoma. Further, glaucoma patients with normal IOP show clear evidence for cerebral and ocular ischemia. Aging and atherosclerosis reduce the ability of the eye to autoregulate blood flow when ocular perfusion pressure changes: the dependence of blood flow on perfusion pressure links ischemia to IOP. Consequently, neuroprotective treatments for glaucoma should be designed to both reduce IOP and improve ocular nutrient delivery.
除眼压升高之外的其他因素必定参与了青光眼的发生和发展。疾病病因中的另一个因素可能是视网膜和视神经乳头的缺血。中枢神经系统神经元的缺血性损伤在机制和组织病理学上与青光眼所见的变化相似。此外,眼压正常的青光眼患者有明显的脑和眼部缺血证据。衰老和动脉粥样硬化会降低眼睛在眼灌注压变化时自动调节血流的能力:血流对灌注压的依赖性将缺血与眼压联系起来。因此,青光眼的神经保护治疗应旨在降低眼压并改善眼部营养物质供应。