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Einar Stefansson, MD, PhD; David Robinson; Myron L. Wolbarsht, PhD; Maurice B. Landers III, MD; Arthur Walsh

Arch Ophthalmol. 1983;101(4):636-639.

Abstract
• A polarographic oxygen electrode was inserted through the cornea into the middle of the anterior chamber, and the aqueous humor Po₂ was continuously monitored. Epinephrine hydrochloride applied topically to the cornea (1% Epifrin: 0.05 to 0.1 mL) or injected into the anterior chamber (Adrenalin Chloride: 1 mg/mL, 0.05 mL) caused a marked decrease in the anterior chamber Po₂. This drop in anterior chamber Po₂ was not simply due to mydriasis, since atropine sulfate administered in a similar fashion did not cause a notable drop in anterior chamber Po₂, and epinephrine applied to eyes with the pupils previously dilated with atropine still caused the typical drop in anterior chamber Po₂. The hypoxic effects of epinephrine were reversed by injection of an -adrenergic blocker, phentolamine mesylate (5 mg/mL, 0.05 mL), into the anterior chamber.

Author Affiliations
From the Departments of Ophthalmology (Drs Stefansson, Wolbarsht, and Landers and Messrs Robinson and Walsh) and Biomedical Engineering (Mr Walsh), Duke University, Durham, NC. Dr Stefansson is a Fellow of the Fogerty International Center.

Footnotes
Accepted for publication April 12, 1982.

Reprint requests to Department of Ophthalmology, Duke University Medical Center, Box 3802, Durham, NC 27710 (Dr Landers).

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