May 2006
Volume 47, Issue 13
ARVO Annual Meeting Abstract  |   May 2006
Pilocarpine–Induced Flare Is Physiological Rather Than Pathological
Author Affiliations & Notes
  • N. Neville
    Department of Bioscience, New England College of Optometry, Boston, MA
  • T.F. Freddo
    Department of Bioscience, New England College of Optometry, Boston, MA
    Departments of Ophthalmology and Pathology, Boston University School of Medicine, Boston, MA
  • Footnotes
    Commercial Relationships  N. Neville, None; T.F. Freddo, None.
  • Footnotes
    Support  NEI Grant # EY–13825 (TFF), Fight for Sight Summer Research Award (NN).
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 212. doi:
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      N. Neville, T.F. Freddo; Pilocarpine–Induced Flare Is Physiological Rather Than Pathological . Invest. Ophthalmol. Vis. Sci. 2006;47(13):212.

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

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Purpose: : Recent studies in humans, using magnetic resonance imaging, showed that the pilocarpine (pilo) induced elevation of aqueous humor protein level is not the result of breakdown of the blood–aqueous barrier (BAB) in the ciliary body. These non–invasive, direct observations of BAB kinetics in the posterior chamber of the eye stand in contrast to prior reports of BAB breakdown, and raise the novel prospect that clinical flare can arise through physiological and not only pathological means. The purpose of these studies was to explore possible physiological sources of the pilo–induced flare response.

Methods: : Seven adult pigmented rabbits of either sex were used. In all animals, initial measurements of pupil size and anterior chamber flare were made (Kowa Flare–cell meter). One eye then received a single drop of 3% pilo. After an hr, these measurements were repeated. Four of the animals then received an i.v. injection of 250 mg/kg of horseradish peroxidase (HRP), which circulated for 3 minutes prior to sacrifice. Eyes were enucleated, uvea carefully dissected, and 150µm sections were reacted for HRP distribution. The remaining 3 animals received no HRP. Their eyes were enucleated, uvea gently dissected, cut into quadrants, and the iris cut from the ciliary body. Two iris quadrants were weighed and placed in 1 ml of PBS, gently agitated in the cold for 4 hrs, and total soluble protein was then measured in the eluant. Remaining quadrants were immunohistochemically examined for the distribution of albumin.

Results: : One hr after pilo, pupil size (mm/SD) was reduced from 6.64/0.6 to 4.36/0.6 and flare (photons/ms/SD) increased from 3.9 /0.6 to 29.4/7.9 (p<0.0001 for each). No HRP leakage was found across the ciliary epithelium or iris vascular endothelium in pilo or control eyes. Immunohistochemistry readily demonstrated albumin staining in the iris and ciliary body stromas in all eyes. In iris specimens from pilo treated eyes an average of 28% less soluble protein was eluted from the iris stroma than in contralateral iris controls.

Conclusions: : Our studies confirmed the presence of a reservoir of plasma–derived protein in the iris stroma. The HRP studies confirm recent MRI studies in humans showing that the source of pilocaprine–induced flare is not disruption of the ciliary epithelial barrier, extending this work by also excluding iris vascular leakage as a source of the flare. Instead, a primary source of pilo–induced flare appears to be the partial extrusion of the iris stromal protein reservoir brought on by thinning of the iris stroma during pilo–induced miosis.

Keywords: iris 

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