Vascular theory of the pathogenesis of glaucomatous optic neuropathy: vascular dysregulation, rheology, ocular perfusion pressure, intraocular and systemic hemodynamics. Report 1

Glaucomatous optic neuropathy (GON) in primary openangle glaucoma (POAG), including normal-tension glaucoma (NTG), is a multifactorial disease in which vascular mechanisms play a significant role. This article reviews current Russian and international literature on the vascular theory of GON. Impaired autoregulation of ocular blood flow, vasospasm, endothelial dysfunction with increased production of endothelin-1, reduced levels of nitric oxide and alterations in its metabolism may contribute to glaucomatous damage to the optic nerve even at normal intraocular pressure levels. The review examines the role of ocular perfusion pressure, hemorheological properties of blood, and systemic hemodynamics, including blood pressure variability, as potentially significant risk factors for the development and progression of GON. Several studies confirm reduced ocular blood flow and the presence of microvascular disturbances in patients with NTG independent of intraocular pressure. The paper also discusses changes in blood viscosity, aggregation of formed elements and their impact on microcirculation in ocular structures. The study concludes that there is a high likelihood of vascular involvement in the pathogenesis of GON, emphasizing the need for a comprehensive approach to the diagnosis and management of patients with POAG.