INTRODUCTION: Acute exposure to hypoxic environments, such as high altitude, can lead to transient or lasting visual disturbances, including high-altitude retinopathy (HAR). These conditions arise from disrupted neurovascular regulation and impaired oxygen delivery to neural tissues. The retina is highly vulnerable to hypoxia, as is the visual cortex, making the visual system a sensitive readout of hypoxia-induced neurodegeneration.

AIM(S): In this study, we used a rat model of acute hypobaric hypoxia to examine how oxygen deprivation alters retinal cytoarchitecture and neurovascular integrity, and whether corticosteroid intervention can modify these effects.

METHOD(S): Animals were exposed to a simulated high altitude environment, with a subset receiving dexamethasone pretreatment. Hypoxic injury was induced in a hypobaric chamber (FiO₂ = 16.6%) for 6 hours/day over 3 days. Animals in the treatment group received a single intraperitoneal dose of dexamethasone (1 mg/kg) before hypoxic exposure. Histomorphological and ultrastructural analyses have been utilized to reveal hypoxia-associated cellular injury and the modulatory effect of the corticosteriod pretreatment.

RESULTS: Hypoxic exposure resulted in marked structural remodeling of the inner retina, including thickening of the ganglion cell and nerve fiber layers, vascular leakage, and neuronal swelling, accompanied by degenerative changes in the visual cortex. In contrast, dexamethasone pretreatment attenuated inflammatory responses, preserved barrier integrity, and maintained retinal and cortical neuronal organization.

CONCLUSIONS: These findings demonstrate that acute hypoxia rapidly reshapes retinal structure through inflammatory and neurovascular mechanisms, and that pharmacological modulation can partially restore neural integrity. HAR may therefore provide a useful experimental framework for studying hypoxia-driven neurodegeneration across the visual system.

FINANCIAL SUPPORT: The work was supported by the Higher Education and Science Committee of MESCS RA (Research project №. 25RG-1F181).