October 1969
Volume 8, Issue 5
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Articles  |   October 1969
The Effect of Corticosteroids on Aqueous Humor Formation Rate and Outflow Facility
Author Affiliations
  • W. W. OPPELT
    Department of Pharmacology and Therapeutics, University of Florida College of Medicine, Gainesville, Fla. 32601; Burroughs Wellcome Scholar in Clinical Pharmacology
  • E.D. WHITE, Jr.
    Department of Pharmacology and Therapeutics, University of Florida College of Medicine, Gainesville, Fla. 32601
  • E.S. HALPERT
    Department of Pharmacology and Therapeutics, University of Florida College of Medicine, Gainesville, Fla. 32601
Investigative Ophthalmology & Visual Science October 1969, Vol.8, 535-541. doi:
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      W. W. OPPELT, E.D. WHITE, E.S. HALPERT; The Effect of Corticosteroids on Aqueous Humor Formation Rate and Outflow Facility. Invest. Ophthalmol. Vis. Sci. 1969;8(5):535-541.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

The effect of corticosteroids on aqueous humor (AH) formation rate and outflow facility was measured in the cat eye. AH formation rate was determined by continuous posteroanterior chamber perfusion with an AH-like buffer containing inulin-C14. It was found that the total quantity of inulin-C14 recovered through the anterior chamber outflow cannula could be used to estimate changes in outflow facility. Intravenous hydrocortisone in doses from 1 to 100 mg. per kilogram caused a dose-related decrease in AH formation rate. At the same doses and at 0.1 mg. per kilogram, there was a decrease in outflow facility averaging about 23 percent. When various doses of hydrocortisone were perfused through the eye chambers or injected into the vitreous, there was no change in AH formation rate or outflow facility. When hydrocortisone or dexamethasone was dropped onto the cornea, there was again a slight reduction in AH formation rate and a significant decrease in outflow facility. Particularly with dexamethasone, the effect on the outflow facility seemed to predominate over the effect on AH formation rate. Data suggest that the rise in intraocular pressure reported after topical or systemic corticosteroids is mediated by a direct effect of these hormones on the outflow facility. The outflow facility appears to be more sensitive to corticosteroids than the mechanism controlling AH secretion.

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