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B. Seitz, Z. Gatzioufas, P. Charalambous, U. Loew, F. Schirra, S. Thanos; Dysfunctional Uveoscleral Pathway in a Rat Model of Congenital Glaucoma. Invest. Ophthalmol. Vis. Sci. 2009;50(13):4849.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate the presence of the uveoscleral pathway in a normotensive rat as well as in a rat model of elevated intraocular pressure (IOP) resembling human inherited buphthalmos.
We injected the fluorescent tracer 70-kDa dextran rhodamine B in the anterior chamber of four eight-week-old normotensive Sprague Dawley rats and four eight-week-old rats with increased IOP manifesting features of congenital glaucoma (CG). IOP was measured with the aid of Tonopen-XL 1 hour before the injection. After survival times of 10 and 60 minutes the rats were euthanized by CO2 inhalation, the eyes were enucleated and cryosections were prepared. These sections were observed by fluorescence microscopy.
IOP in the CG group was significantly increased (29.5±3.4 mmHg) compared to the control group (12.7±2.7 mmHg) (Fisher exact test, p<0.001). Histological examination confirmed the presence of an open irido-corneal angle in the CG group. Fluorescent tracer was detected in the iris root and ciliary processes in both groups of rats after 10 minutes. Nonetheless, after 60 min the signal intensity was prominent in the choroid of the normotensive rats, whereas the fluorescent staining in the sclera and choroid of rats with CG was almost absent.
Our results document the presence of an uveoscleral pathway in the normotensive rat and also indicate a severe impairment of the uveoscleral pathway in the rat model of CG, suggesting that reduced uveoscleral outflow might play a role in the pathogenesis of CG.
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