Objectives： Ocular effects of Mas-receptor ligands were studied in an experimental rat glaucoma. Elevated IOP （intraocular pressure） was induced unilaterally by laser photocoagulation of the episcleral and limbal v...Objectives： Ocular effects of Mas-receptor ligands were studied in an experimental rat glaucoma. Elevated IOP （intraocular pressure） was induced unilaterally by laser photocoagulation of the episcleral and limbal veins in anesthetized rats. A Mas-receptor agonist （Ang （1-7）） and an antagonist （A779） were administered intravitreally in the glaucomatous eye. lOP was measured by a rebound tonometer. Effects of the treatment on RGCL （retinal ganglion cell layer） were determined stereologically and on the axons of optic nerve by a modified Gallyas silver-staining method. Key findings： Mean IOP during the 14 days follow-up in the solvent treated glaucoma eyes （n = 18） was 28.7 -4- 1.9 mmHg vs. the fellow eyes 11.0 4- 0.3 mmHg. A significant axon damage was detected in the glaucomatous eyes vs. the fellow normotensive eye. The Mas-receptor ligands did not influence high IOP resulted by laser treatment, Despite of the ineffectiveness on lOP, Ang （1-7） protected RGCL cells as determined by stereology （P = 0.016）. No significant effects in Gallyas silver-staining were found. Summary： Intravitreally administered Ang （1-7） showed a significant protective effect against neuronal damage. The present and our previous studies suggest that stimulation of Mas-receptor may have therapeutic potential to treat glaucoma.展开更多
Objective To develop and evaluate the rat model of chronic glaucoma by episcleral veins ligation （EVL）. Methods Experimental glaucoma was induced unilaterally in 28 male Sprague-Dawley rats by ligating two episclera...Objective To develop and evaluate the rat model of chronic glaucoma by episcleral veins ligation （EVL）. Methods Experimental glaucoma was induced unilaterally in 28 male Sprague-Dawley rats by ligating two episcleral veins. Intraocular pressure （10P） in rats was measured by a Goldmann applanation tonometer under 3 % pentobarbital sodium anesthesia. The optic nerve head and retinal vasculature were assessed by repeated fundus examinations. The amount of optic nerve axons was assessed by Image-Pro Plus image analysis system in a masked fashion. Results lOP without EVL was （ 19.21 ± 1.23） mmHg, whereas the EVL eyes gained about 1.8-fold higher 10P[ （33.96 ±2. 73） mmHg]after EVL immediately （ P 〈 0. 001 ）. The elevated IOP gradually decreased over time. However, the differences were kept significant up to 8 weeks after EVL. The lOP was reduced to similar levels as contralateral eyes at 12 and 16 weeks after EVL. The glaucomatous optic nerve excavation appeared in EVL eyes at 8 weeks after EVL, and the optic nerve excavation enlarged gradually with the increasing post-operation time. The amount of optic nerve axons also significantly decreased in EVL eyes at 8 weeks after EVL, and the amount of axons decreased gradually with the increasing post-operation time. Conclusion Increase of lOP caused by EVL represents a useful and efficient model of experimental glaucoma in rats.展开更多
文摘Objectives： Ocular effects of Mas-receptor ligands were studied in an experimental rat glaucoma. Elevated IOP （intraocular pressure） was induced unilaterally by laser photocoagulation of the episcleral and limbal veins in anesthetized rats. A Mas-receptor agonist （Ang （1-7）） and an antagonist （A779） were administered intravitreally in the glaucomatous eye. lOP was measured by a rebound tonometer. Effects of the treatment on RGCL （retinal ganglion cell layer） were determined stereologically and on the axons of optic nerve by a modified Gallyas silver-staining method. Key findings： Mean IOP during the 14 days follow-up in the solvent treated glaucoma eyes （n = 18） was 28.7 -4- 1.9 mmHg vs. the fellow eyes 11.0 4- 0.3 mmHg. A significant axon damage was detected in the glaucomatous eyes vs. the fellow normotensive eye. The Mas-receptor ligands did not influence high IOP resulted by laser treatment, Despite of the ineffectiveness on lOP, Ang （1-7） protected RGCL cells as determined by stereology （P = 0.016）. No significant effects in Gallyas silver-staining were found. Summary： Intravitreally administered Ang （1-7） showed a significant protective effect against neuronal damage. The present and our previous studies suggest that stimulation of Mas-receptor may have therapeutic potential to treat glaucoma.
基金Supported by Shanghai Education Committee Project Foundation (06BZ040)
文摘Objective To develop and evaluate the rat model of chronic glaucoma by episcleral veins ligation （EVL）. Methods Experimental glaucoma was induced unilaterally in 28 male Sprague-Dawley rats by ligating two episcleral veins. Intraocular pressure （10P） in rats was measured by a Goldmann applanation tonometer under 3 % pentobarbital sodium anesthesia. The optic nerve head and retinal vasculature were assessed by repeated fundus examinations. The amount of optic nerve axons was assessed by Image-Pro Plus image analysis system in a masked fashion. Results lOP without EVL was （ 19.21 ± 1.23） mmHg, whereas the EVL eyes gained about 1.8-fold higher 10P[ （33.96 ±2. 73） mmHg]after EVL immediately （ P 〈 0. 001 ）. The elevated IOP gradually decreased over time. However, the differences were kept significant up to 8 weeks after EVL. The lOP was reduced to similar levels as contralateral eyes at 12 and 16 weeks after EVL. The glaucomatous optic nerve excavation appeared in EVL eyes at 8 weeks after EVL, and the optic nerve excavation enlarged gradually with the increasing post-operation time. The amount of optic nerve axons also significantly decreased in EVL eyes at 8 weeks after EVL, and the amount of axons decreased gradually with the increasing post-operation time. Conclusion Increase of lOP caused by EVL represents a useful and efficient model of experimental glaucoma in rats.
