Competing/conflicts of interest: No stated conflict of interest.
Experimental chronic ocular hypertension by anterior chamber injection of 0.3% carbomer solution in the rat
Version of Record online: 21 NOV 2012
© 2012 The Authors. Clinical and Experimental Ophthalmology © 2012 Royal Australian and New Zealand College of Ophthalmologists
Clinical & Experimental Ophthalmology
Volume 41, Issue 4, pages 404–412, May/June 2013
How to Cite
Kim, H.-G., Park, J.-W. and Park, S.-W. (2013), Experimental chronic ocular hypertension by anterior chamber injection of 0.3% carbomer solution in the rat. Clinical & Experimental Ophthalmology, 41: 404–412. doi: 10.1111/j.1442-9071.2012.02883.x
Funding sources: No stated funding sources.
- Issue online: 5 JUN 2013
- Version of Record online: 21 NOV 2012
- Accepted manuscript online: 25 SEP 2012 07:50AM EST
- Manuscript Accepted: 5 SEP 2012
- Manuscript Received: 20 MAR 2012
- animal model;
- retinal ganglion cell
To evaluate a chronic ocular hypertensive model by anterior chamber injection of 0.3% carbomer solution in rats.
Chronic ocular hypertension was induced unilaterally by injecting 20 μL of 0.3% carbomer solution into the anterior chamber in 3-month-old Sprague Dawley rats. Intraocular pressure was measured everyday for 1 week and then every week for 2 months after a single or repeated injection. Retinal ganglion cell loss was assessed quantitatively using FluoroGold labelling at 2, 4 and 8 weeks after injection. Anterior chamber angle and optic nerve were examined after chronic intraocular pressure elevation.
The mean and peak intraocular pressure of the injected eyes were elevated significantly higher than those of the control eyes for 6 weeks of the experiment, after a single injection of carbomer solution and a second injection at 2 weeks resulted in an 8-week elevation of the mean and peak intraocular pressure, which was significantly higher than those of the control eyes. Elevated intraocular pressure induced retinal ganglion cell loss by approximately 21%, 27% and 38% compared with that in the control eyes at 2, 4 and 8 weeks, respectively, after a single injection. In carbomer-injected eyes with chronic intraocular pressure elevation, the obstruction of anterior chamber angle by peripheral anterior synechia and optic nerve degeneration were observed.
Anterior chamber injection of 0.3% carbomer solution was an effective and reproducible method to produce chronic intraocular pressure elevation and glaucomatous neurodegeneration in rats.