Objective To study the retinal tissue degeneration of intraocular hypertension experimentally induced in acute and chronic way. Methods In the acute model, pressure elevation was quickly induced by a needle in the ant...Objective To study the retinal tissue degeneration of intraocular hypertension experimentally induced in acute and chronic way. Methods In the acute model, pressure elevation was quickly induced by a needle in the anterior chamber and the retinal reaction was studied at 1,2,4,5,7,10 days after treatment. The tissue damage with chronic hypertension,induced by the cauterization of two episcleral veins,was studied at 1 and 2 month after the treatment. The TUNEL method and Caspade 3a immunochemical study evidenced the apoptosis mechanism. The NADPH-diaphorase reaction identified the Nitric Oxide, ( NO) producing cells. Results In the acute model,the immunohistochemical study evidenced that the apoptosis was an early death mechanism for ganglionar cells. The activity of Nitric Oxide Synthase ( NOS) didn' t show a significant activation toward the retinal tissue of control. The chronic hypertension model indicated an increase in the NOS signal, meaning an activation of this enzyme in particular bear the vascular vessels, showing the neuroprotective and not only cytotoxic effect of the NO. The TUNEL and Caspase 3a studies indicated that the apoptosic mechanism started in different times, the immunohistochemical reaction showed its immediately beginning or its later activation caused by the chronic damage. Conclusions The opportunity to have a clear vision of the beginning and causing factors of cell degeneration in hypertension damage could permit the study on different substances that act on apoptosis , on NOS mechanism and on synaptic transmission inhibiting or deviating the retinal tissue degeneration and particularly the ganglionar cells death in glaucoma.展开更多
文摘Objective To study the retinal tissue degeneration of intraocular hypertension experimentally induced in acute and chronic way. Methods In the acute model, pressure elevation was quickly induced by a needle in the anterior chamber and the retinal reaction was studied at 1,2,4,5,7,10 days after treatment. The tissue damage with chronic hypertension,induced by the cauterization of two episcleral veins,was studied at 1 and 2 month after the treatment. The TUNEL method and Caspade 3a immunochemical study evidenced the apoptosis mechanism. The NADPH-diaphorase reaction identified the Nitric Oxide, ( NO) producing cells. Results In the acute model,the immunohistochemical study evidenced that the apoptosis was an early death mechanism for ganglionar cells. The activity of Nitric Oxide Synthase ( NOS) didn' t show a significant activation toward the retinal tissue of control. The chronic hypertension model indicated an increase in the NOS signal, meaning an activation of this enzyme in particular bear the vascular vessels, showing the neuroprotective and not only cytotoxic effect of the NO. The TUNEL and Caspase 3a studies indicated that the apoptosic mechanism started in different times, the immunohistochemical reaction showed its immediately beginning or its later activation caused by the chronic damage. Conclusions The opportunity to have a clear vision of the beginning and causing factors of cell degeneration in hypertension damage could permit the study on different substances that act on apoptosis , on NOS mechanism and on synaptic transmission inhibiting or deviating the retinal tissue degeneration and particularly the ganglionar cells death in glaucoma.
