Iris vasculopathy in galactose-fed rats

Laure E. Caspers-Velu, Kishena C. Wadhwani, Stanley I. Rapoport, Peter F. Kador

Research output: Contribution to journalArticle

4 Scopus citations

Abstract

Increased iris vessel permeability observed in diabetics has also been reported to occur in diabetic animals and galactose-fed rats. The potential role of aldose reductase in the induction of iris vessel-changes has been investigated in rats fed a 50% galactose diet with/without the aldose reductase inhibitors AL 1576, sorbinil or ponalrestat for 7 to 18 months. Compared to normal control rats, long-term galactose-fed rats display a breakdown of the blood-aqueous barrier due to iris vessel changes that include focal straightening, dilation, constriction, increased permeability, ischemia and new vessel proliferation. The onset and progression of these iridal vessel changes were prevented by the aldose reductase inhibitors AL 1576 and sorbinil, and reduced by Ponalrestat. Computerized analyses of lumen areas of iris vessels indicated an 18-fold decrease in the vascular area near the pupillary boarder in untreated galactose-fed rats compared with age- matched controls and galactose-fed rats treated with aldose reductase inhibitors. These observations linking iris vessel changes with galactose- feeding, coupled with the fact that aldose reductase inhibitors also prevent these changes, strongly suggest a link between the sorbitol pathway and the appearance and progression of iris vessel changes.

Original languageEnglish (US)
Pages (from-to)211-221
Number of pages11
JournalExperimental Eye Research
Volume68
Issue number2
DOIs
StatePublished - Feb 1999

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Keywords

  • Blood vessels
  • Blood-aqueous barrier
  • Diabetes
  • Galactose
  • Permeability

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience

Cite this

Caspers-Velu, L. E., Wadhwani, K. C., Rapoport, S. I., & Kador, P. F. (1999). Iris vasculopathy in galactose-fed rats. Experimental Eye Research, 68(2), 211-221. https://doi.org/10.1006/exer.1998.0594