Edema and increased endoneurial sodium in galactose neuropathy. Reversal with an aldose reductase inhibitor.

Galactose neuropathy was produced in rats by feeding a diet containing 30% D-galactose. After 12 weeks of galactose ingestion, all rats developed bilateral cataracts, polydypsia and polyuria. These galactose-intoxicated animals were divided into two groups that both continued with the galactose diet: animals that were treated with the aldose reductase inhibitor, ICI 128,436, for 4-6 weeks, and a control group of animals that received just excipient. At the end of the study, endoneurial fluid pressures, nerve water contents and endoneurial fluid electrolyte concentrations were determined from sciatic nerves of treated and untreated animals. The extent of neuropathy in each animal was evaluated by light microscopy. Treatment of galactose-intoxicated rats with ICI 128,436 restored to normal levels the elevated endoneurial sodium concentration, increased water content and interstitial fluid pressure characteristic of galactose neuropathy. These results, obtained with an agent that blocks the sorbitol pathway, associate elevated sodium with an osmotic force contributing to edema and increased endoneurial fluid pressure in galactose neuropathy and suggest that endoneurial sodium levels are linked to blood-sugar concentration.