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Iris Stiffening Following Drug Stimulation

[+] Author Affiliations
Julie E. Whitcomb, Vincent A. Barnett, Timothy W. Olsen, Victor H. Barocas

University of Minnesota, Minneapolis, MN

Paper No. SBC2007-176013, pp. 885-886; 2 pages
doi:10.1115/SBC2007-176013
From:
  • ASME 2007 Summer Bioengineering Conference
  • ASME 2007 Summer Bioengineering Conference
  • Keystone, Colorado, USA, June 20–24, 2007
  • Conference Sponsors: Bioengineering Division
  • ISBN: 0-7918-4798-5
  • Copyright © 2007 by ASME

abstract

Glaucoma is a general term for the deterioration of the optic nerve head usually associated with an increase of intraocular pressure (IOP). Certain types of glaucoma are associated directly with the displacement of the iris from its normal morphology [1]. For example, angle closure glaucoma and pigment dispersion syndrome involve abnormal anterior or posterior displacement of the iris, respectively [2]. In angle closure, the abnormal position of the peripheral iris blocks aqueous humor access to the outflow pathway (trabecular meshwork), increasing the IOP. Although there has been a considerable amount of ultrastructural characterization of the iris [3], to our knowledge, there as been little done on the mechanical characterization of the iris other than a previous study by Heys and Barocas on passive bovine irides [4]. To have a complete understanding of these it requires that we understand the mechanical properties of the iris in both its passive and stimulated states. Mechanical analysis of the iris requires the consideration of its two constituent muscles, the inner sphincter iridis and the outer dilator pupillae, see Fig. 1. The sphincter iridis is innervated parasympathetically whereas the dilator is innervated sympathetically.

Copyright © 2007 by ASME

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