November 1990
Volume 31, Issue 11
Free
Articles  |   November 1990
Corneal hydration control in normal and alloxan-induced diabetic rabbits.
Author Affiliations
  • P R Herse
    Department of Optometry, University of Auckland, NZ.
Investigative Ophthalmology & Visual Science November 1990, Vol.31, 2205-2213. doi:
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      P R Herse; Corneal hydration control in normal and alloxan-induced diabetic rabbits.. Invest. Ophthalmol. Vis. Sci. 1990;31(11):2205-2213.

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Abstract

Reports of increased corneal thickness and altered endothelial morphology suggest that there is abnormal corneal hydration control in diabetic patients. To study the possible influence of hyperglycemia on corneal hydration control, experiments were done on normal and alloxan-induced diabetic rabbits to assess: (1) stromal dry weight, hydration, and swelling pressure; (2) corneal thickness and contact lens-induced edema recovery responses; and (3) endothelial homogenate sodium/potassium adenosinetriphosphatase (Na+/K+ ATPase) activity. The data show that 10 weeks of uncontrolled hyperglycemia in the rabbit results in abnormal corneal hydration control indicated by increased corneal thickness, increased stromal hydration, and a decreased ability to recover from contact lens-induced corneal edema. The stroma appears to be minimally involved in these changes; swelling pressures and dry weights of the normal and diabetic stroma were not significantly different. The measured decrease in diabetic rabbit endothelial homogenate Na+/K+ ATPase activity strongly suggests that endothelial fluid pump dysfunction is a major component in the abnormal corneal hydration control found in the uncontrolled diabetic rabbit.

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