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Experimental chronic ocular hypertension by anterior chamber injection of 0.3% carbomer solution in the rat


  • Competing/conflicts of interest: No stated conflict of interest.
  • Funding sources: No stated funding sources.

Correspondence: Dr Sang-Woo Park, Department of Ophthalmology, Chonnam National University Medical School and Hospital, Chonnam National Research Institute for Medical Sciences, #8 Hak-dong, Dong-gu, Gwangju 501-757, South Korea. Email:



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.