Nerve water content and the permeability–surface area product (PA) to [3H]- or [14C]sucrose at the blood-nerve barrier were determined in unanesthetized control rats fed a normal diet and in rats fed galactose with or without an aldose reductase inhibitor (Statil or AL 1576) or a thromboxane synthetase inhibitor (CGS 12970). Nerve water content was determined by taking the difference between dry and wet weights of whole tibial nerves. PA was determined by an intravenous bolus injection of radiotracer with multiple–time-point graphic and quantitative autoradiographic methods. The mean nerve water content in galactosemic rats was 15% higher than in control rats after 7–11 mo on the diet. Statil and AL 1576 prevented nerve edema, but CGS 12970 was only partially effective in preventing an increase in nerve water content in galactose-fed rats. In galactosemic rats, the mean PA to sucrose at the blood-nerve barrier, calculated from nerve dry weight, was twofold higher than in control rats. Treatment with Statil, AL 1576, or CGS 12970 prevented increased PA. Our results suggest that nerve edema and increased blood-nerve barrier PA are secondary to polyol production and can be prevented by inhibiting aldose reductase.
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Original Articles|
November 01 1989
Prevention of Nerve Edema and Increased Blood-Nerve Barrier Permeability–Surface Area Product in Galactosemic Rats by Aldose Reductase or Thromboxane Synthetase Inhibitors
Kishena C Wadhwani;
Kishena C Wadhwani
Laboratory of Neurosciences, National Institute on Aging, and the Laboratory of Mechanisms of Ocular Diseases, National Eye Institute, National Institutes of Health
Bethesda, Maryland
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Laure E Caspers-Velu;
Laure E Caspers-Velu
Laboratory of Neurosciences, National Institute on Aging, and the Laboratory of Mechanisms of Ocular Diseases, National Eye Institute, National Institutes of Health
Bethesda, Maryland
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Vincent A Murphy;
Vincent A Murphy
Laboratory of Neurosciences, National Institute on Aging, and the Laboratory of Mechanisms of Ocular Diseases, National Eye Institute, National Institutes of Health
Bethesda, Maryland
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Quentin R Smith;
Quentin R Smith
Laboratory of Neurosciences, National Institute on Aging, and the Laboratory of Mechanisms of Ocular Diseases, National Eye Institute, National Institutes of Health
Bethesda, Maryland
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Peter F Kador;
Peter F Kador
Laboratory of Neurosciences, National Institute on Aging, and the Laboratory of Mechanisms of Ocular Diseases, National Eye Institute, National Institutes of Health
Bethesda, Maryland
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Stanley I Rapoport
Stanley I Rapoport
Laboratory of Neurosciences, National Institute on Aging, and the Laboratory of Mechanisms of Ocular Diseases, National Eye Institute, National Institutes of Health
Bethesda, Maryland
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Address correspondence and reprint requests to Kishena C. Wadhwani, PhD, Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health Building 10, Room 6C103, Bethesda, MD 20892.
Diabetes 1989;38(11):1469–1477
Article history
Received:
March 17 1989
Revision Received:
July 12 1989
Accepted:
July 12 1989
PubMed:
2559867
Citation
Kishena C Wadhwani, Laure E Caspers-Velu, Vincent A Murphy, Quentin R Smith, Peter F Kador, Stanley I Rapoport; Prevention of Nerve Edema and Increased Blood-Nerve Barrier Permeability–Surface Area Product in Galactosemic Rats by Aldose Reductase or Thromboxane Synthetase Inhibitors. Diabetes 1 November 1989; 38 (11): 1469–1477. https://doi.org/10.2337/diab.38.11.1469
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