Active transport system of prostaglandins: clinical implications and considerations

J Cataract Refract Surg. 1992 Jan;18(1):100-5. doi: 10.1016/s0886-3350(13)80390-2.

Abstract

We hypothesize that two factors are essential in the development of epinephrine-induced cystoid macular edema (CME): (1) the stimulation of prostaglandin synthesis by some tissues, presumably the anterior uvea by epinephrine; (2) the dysfunction of the active transport (Bito's pump) which is responsible for the removal of prostaglandins from intraocular fluids. We conducted several experimental studies to confirm these hypotheses. The results strongly suggest that epinephrine maculopathy is induced by a mechanism involving prostaglandins or, possibly, other related eicosanoids and not simply by epinephrine itself, as has been postulated. This suggests the existence of some common factors in the pathogenesis of epinephrine maculopathy and aphakic or pseudophakic CME.

Publication types

  • Review

MeSH terms

  • Animals
  • Aqueous Humor / metabolism
  • Biological Transport, Active
  • Blood / metabolism
  • Blood-Retinal Barrier
  • Cataract Extraction / adverse effects
  • Epinephrine / adverse effects
  • Humans
  • Macular Edema / chemically induced
  • Macular Edema / metabolism*
  • Prostaglandins / metabolism*
  • Rabbits

Substances

  • Prostaglandins
  • Epinephrine