Mexidol in the complex treatment of glaucoma

Author:
E.A. EGOROV, N.G. DAVYDOVA, I.A. ROMANENKO, N.D. NOVIKOVA

RNIMU named after N.I. Pirogov, GB of GB named after Helmholtz, Moscow

Place of publication:
CLINICAL OPHTHALMOLOGY VOL. 12, No. 3, 2011

Abstract:
Primary open-angle glaucoma (POAG) remains a major medical and social issue. Glaucoma is a leading cause of blindness in developed countries, making improved diagnosis and treatment of this disease extremely pressing. The etiopathogenesis of glaucoma is complex and, despite numerous studies, remains unclear. There is every reason to believe it is multifactorial. Glaucoma optic neuropathy (GON) is caused by various factors leading to retinal ganglion cell apoptosis: pressure of optic nerve axons within the openings of the lamina cribrosa, posterior displacement due to elevated intraocular pressure (IOP), impaired blood supply to the optic nerve head, excess free radical formation due to ischemia, and increased lipid peroxidation (LPO). During ischemia, protein synthesis in nerve tissue is inhibited and anaerobic glycolysis is activated. Subsequently, the K-Na pump is disrupted, leading to depolarization of cell membranes. In response, glutamate is released, which activates neurons via NMDA receptors, leading to an excess of calcium ions entering the cell. Excessively high Ca2+ concentrations in cells trigger the activation of complex cascades of nucleases, proteases, and lipases. These directly affect intracellular proteins and lipids, resulting in the formation of reactive free radicals and excessive nitric oxide (NO), which can contribute to the development of gonadotropin-negative syndrome (GNS). Various reactive oxygen species are formed, which have a cytotoxic effect on the retina and optic nerve, leading to destructive changes in the drainage system. Essentially, mechanical and vascular factors exert their effects through metabolic processes.