SUMMARY
Introduction. Glutamate exitotoxicity plays a leading role in damaging of the visual analyzer of traumatic genesis. As it was shown recently, hydrogen sulfide (H2S) system is involved in the regulation of neurotransmission, ophthalmotonus and retinal injury, but its role in the pathogenesis of post-traumatic injury of the visual analyzer has not been clarified.The aim of the study – to evaluate the association of neuroretinal destruction markers with retinal level of hydrogen sulfide in experimental traumatic injury of the visual analyzer.Research Methods. Experiments were carried out on 24 male rabbits weighing 3.0–3.9 kg. Traumatic injury of visual analyzer in rabbits was caused by the action of carbon dioxide stream under pressure on the cornea of the eye. The levels of H2S, glutamate, cytometric markers of apoptosis in the retina, and the levels of neuron specific enolase (NSE) and S100 protein in the blood serum were determined.Results and Discussion. Traumatic injury of the visual analyzer in the rabbits was characterized by increase levels of NSE neuronal markers and S100 protein in serum, and increase in glutamate level and the number of cells in the SUB-G0G1 phase (apoptotic marker) in the retina during 24 hours, followed by the escalation of neuroretinodestruction signs in 7 days. After 24 hours after the injury, increase of H2S level (2-times) was observed in retina, but in 7 days its level was significantly decreased (4-times). Formation of H2S deficiency in retina was associated with aggravation of glutamate excitotoxicity and neuroretinal destruction signs.Conclusions. Thus, H2S system is involved in the mechanisms of retina injury in case of contusive eye trauma. H2S level correction in the retina may be a promising strategy in traumatic injury to the visual analyzer and this direction is appropriate for further study.