The pattern of functional impairments and the antioxidative and antiproteolytic status of tear were studied, by experimentally simulating retinal ischemia in rabbits and during treatment with Selecarten. Simulated retinal ischemia resulted in the development of persistent (up to 3 weeks) retinal electrogenetic disorder. Selecarten instillations produced a moderate neuroprotective effect, by positively affecting retinal function early after ischemia stimulation and accelerated the recovery of retinal electrogenesis late after laser coagulation of retinal vessels. The altered metabolic processes were characterized by an increase in the tear antiproteolytic potential. The antioxidative activity and the activity of a2-macroglobulin proteolysis inhibitor increased in the tears of Selecarten-treated rabbits.
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