June 1974
Volume 13, Issue 6
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Articles  |   June 1974
Antagonism of Arachidonic Acid-Induced Ocular Effects by Δ1-Tetrahydrocannabinol
Author Affiliations
  • KEITH GREEN
    W. K. Kellogg Research Laboratories, The Wilmer Institute, The Johns Hopkins University School of Medicine, Baltimore, Md.
  • STEVEN M. PODOS
    Department of Ophthalmology, Washington University School of Medicine, St. Louis, Mo. 63110
Investigative Ophthalmology & Visual Science June 1974, Vol.13, 422-429. doi:
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      KEITH GREEN, STEVEN M. PODOS; Antagonism of Arachidonic Acid-Induced Ocular Effects by Δ1-Tetrahydrocannabinol. Invest. Ophthalmol. Vis. Sci. 1974;13(6):422-429.

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Abstract

Arachidonic acid, 2 per cent, instilled into rabbit eyes, produced a marked elevation of intraocular pressure, aqueous humor protein, and total outflow facility. Δ1-Tetrahydrocannabinol (THC) 10 µg given intravenously to achieve a plasma concentration of about 50 x 10-6 mg. per milliliter, caused a 20 to 25 per cent fall in intraocular pressure, and a small rise in aqueous humor protein and total outflow facility. Arachidonic acid when instilled into the eyes of rabbits given THC sixty minutes previously produced a small, transient increase in intraocular pressure. The protein content of the aqueous humor after both THC and arachidonic acid was about one third that found after arachidonic acid alone. Total outflow facility was slightly greater than that seen with THC alone. Prostaglandin E2, 10 µg given topically to the eye, caused an equally large elevation of intraocular pressure and aqueous humor protein whether or not the rabbits were pretreated with intravenous THC. The results suggested that THC antagonizes the in vivo ocular production of prostaglandin from arachidonic acid.

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