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MILES A. GALIN, M.D.; RICHARD DAVIDSON, M.D.

Arch Ophthalmol. 1962;68(5):633-635.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Urea has been widely accepted as an osmotic ocular hypotensive agent.^1-5 Given intravenously at 1 gm. per kilogram, it rapidly reduces intraocular pressure. Consequently, it has proved dramatically effective in acute angle-closure glaucoma.⁶ However, it has been suggested that urea not be used as a last resort in this disorder, since results are not as impressive in the highly inflamed eye.⁶ This has been attributed to loss of the normal osmotic gradient which exists between blood urea nitrogen and aqueous urea nitrogen. If this gradient is reduced or destroyed, only a small osmotic effect is to be expected.

This communication reports a study to evaluate the ocular hypotensive potential of urea before and after alteration of the blood aqueous barrier by anterior segment inflammation.

Material and Methods

Albino rabbits weighing 2-3 kg. were utilized. In 1 group of animals, a polyethylene catheter was inserted into the marginal . . . [Full Text PDF of this Article]

Author Affiliations
New York

From the Department of Surgery (Ophthalmology) of The New York Hospital-Cornell Medical Center.

Footnotes
Submitted for publication April 23, 1962.

Aided by grant No. B-3010 (Rl) from The National Institutes of Health and a grant from The National Society for the Prevention of Blindness.

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