Background: Neuroprotective approaches are considered to be the most promising among existing modern directions in the development of antiglaucomatous drugs. The aim of the study: The detection of morphofunctional changes in the retina following the chronic increase in intraocular pressure modelled by injection of hyaluronic acid (HA) into anterior eye chamber. Materials and methods: Two groups (intact and experimental) of albino rats (10 animals in each group) were used. In experimental animals 25ml of 1% solution of HA was weekly injected into the anterior eye chamber during 10 weeks. The intraocular pressure (IOP) measurement, electroretinigraphy and histological methods with computer morphometry were used. Results: The intracameral administration of HA leads to a statistically significant increase of IOP up to 23,6±1,33 mm Hg which remains stable during10 weeks. Electroretinography demonstrates the development of dysfunction of both photoreceptor and associative neurons of the retina in the form of a significant decrease in the amplitude of a- and b-waves. Histological changes observed in experimental retinas are characteristic of glaucomatous damage with specific neuronal loss in the ganglion layer and atrophic thinning of the nerve fibers layer. The surviving neurons show signs of a compensatory reaction with hypertrophy of the pericaryons, which is more likely a manifestation of their dendritic plasticity. Conclusion: The model used reproduces morphofunctional changes in the retina characteristic of glaucoma and is adequate for reproducing the hypertensive component of the pathogenesis of this disease.
Background: Neuroprotective approaches are considered to be the most promising among existing modern directions in the development of antiglaucomatous drugs. The aim of the study: The detection of morphofunctional changes in the retina following the chronic increase in intraocular pressure modelled by injection of hyaluronic acid (HA) into anterior eye chamber. Materials and methods: Two groups (intact and experimental) of albino rats (10 animals in each group) were used. In experimental animals 25ml of 1% solution of HA was weekly injected into the anterior eye chamber during 10 weeks. The intraocular pressure (IOP) measurement, electroretinigraphy and histological methods with computer morphometry were used. Results: The intracameral administration of HA leads to a statistically significant increase of IOP up to 23,6±1,33 mm Hg which remains stable during10 weeks. Electroretinography demonstrates the development of dysfunction of both photoreceptor and associative neurons of the retina in the form of a significant decrease in the amplitude of a- and b-waves. Histological changes observed in experimental retinas are characteristic of glaucomatous damage with specific neuronal loss in the ganglion layer and atrophic thinning of the nerve fibers layer. The surviving neurons show signs of a compensatory reaction with hypertrophy of the pericaryons, which is more likely a manifestation of their dendritic plasticity. Conclusion: The model used reproduces morphofunctional changes in the retina characteristic of glaucoma and is adequate for reproducing the hypertensive component of the pathogenesis of this disease.