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Galactose neuropathy: impact of chronic endoneurial edema on nerve blood flow.
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Peripheral neuropathy induced by galactose feeding results in endoneurial edema with increased tissue pressure and ultimate demyelination of nerve fibers. To assess the role of ischemia in the pathogenesis of this neuropathy, nerve blood flow was measured 6 months after the start of galactose
Galactose neuropathy. Permeability studies, mechanism of edema, and mast cell abnormalities.
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Galactose neuropathy is characterized by progressive endoneurial edema manifested by a gradual increase in endoneurial fluid pressure. Edema accumulates via a unique mechanism of osmotic force generated by products of the polyol pathway, synthesized within the endoneurial compartment. This paper
Edema and increased endoneurial sodium in galactose neuropathy. Reversal with an aldose reductase inhibitor.
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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
Peripheral nerve conduction studies in galactose-poisoned rats. Demonstration of increased resistance to ischemic conduction associated with endoneurial edema due to sugar alcohol accumulation.
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Edematous nerves of galactose-poisoned rats had an increased resistance to ischemic conduction block when compared with control animals. Ischemia was caused by cardiac arrest due to intracardiac air embolism in 1 group and by occlusion of the abdominal aorta in another. In these 2 groups of
Taurine prevents galactose-induced cataracts.
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Intact lenses from New Zealand white rabbits were incubated in tissue culture media containing either 5 mM glucose or 5 mM glucose plus 30 mM galactose. The standard media did not contain taurine. Lenses were also cultured in a third medium containing 30 mM galactose plus 0.2 mM taurine. The
Axonal caliber and neurofilaments are proportionately decreased in galactose neuropathy.
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Feeding galactose to rats induces nerve conduction abnormalities, increased levels of nerve galactitol, endoneurial edema, elevated pressure and hypoxia of endoneurial fluid, and pathological abnormalities of nerve fibers. To investigate the cellular mechanisms of the fiber lesions and their
Schwann cell changes and demyelination in chronic galactose neuropathy.
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Dystrophic changes of Schwann cells and demyelination occurred in rats with chronic nerve edema induced by feeding a galactose-rich diet for two years. The mechanism for edema is the sorbitol pathway which generates osmotically active polyols from galactose or glucose. The blood-nerve barrier
Dose-dependence of endoneurial fluid sodium and chloride accumulation in galactose intoxication.
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Endoneurial edema in galactose neuropathy was studied in a colony of Sprague-Dawley rats fed diets containing 0%, 10%, 20% or 40% D-galactose for approx. 200 days. Endoneurial fluid was analyzed by X-ray microanalysis for electrolyte concentration, by microgravimetry of whole nerve segments for
Subfertility and growth restriction in a new galactose-1 phosphate uridylyltransferase (GALT) - deficient mouse model.
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The first GalT gene knockout (KO) mouse model for Classic Galactosemia (OMIM 230400) accumulated some galactose and its metabolites upon galactose challenge, but was seemingly fertile and symptom free. Here we constructed a new GalT gene-trapped mouse model by injecting GalT gene-trapped mouse
Increased endoneurial fluid pressure in galactose neuropathy.
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Edema and increased endoneurial fluid pressure developed in peripheral nerves of rats that received a diet containing 40% galactose during a study of the role of sugar alcohols in producing neuropathy. Fluid pressure was elevated starting in the third month and progressed to a fivefold increase over
The appearance of D-galactosamine-induced hepatitis and generalized edema in adrenalectomized rats.
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In adrenalectomized female rats a single dose of 375 mg D-galactosamine.HCl per kg of body weight produces both hepatitis and generalized edema with ascites. These alterations depend upon the dose and the time interval after injection of the aminosugar. The effect is specific for D-galactosamine;
Relationship between nerve blood flow and intercapillary distance in peripheral nerve edema.
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Some human and experimental neuropathies are characterized by endoneurial edema and increased intercapillary distance (ICD). This may potentially produce chronic endoneurial ischemia. To examine the relationship between nerve blood flow (NBF) and ICD we measured NBF in rats with experimental
Evaluation of ammonia and lidocaine clearance, and galactose elimination capacity of xenoperfused pig livers using a pharmacokinetic analysis.
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BACKGROUND
We introduced the pharmacokinetic method into the functional evaluation of xenogeneic extracorporeal liver perfusion as an artificial liver assist device, and examined the influence of xenogeneic humoral injury on the metabolic function of xenoperfused pig livers.
METHODS
Isolated pig
Cloning and sequencing of a Shiga-like toxin type II variant from Escherichia coli strain responsible for edema disease of swine.
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A Shiga-like toxin type II variant (SLT-IIv) is produced by strains of Escherichia coli responsible for edema disease of swine and is antigenically related to Shiga-like toxin type II (SLT-II) of enterohemorrhagic E. coli. However, SLT-IIv is only active against Vero cells, whereas SLT-II is active
Prevention of nerve edema and increased blood-nerve barrier permeability-surface area product in galactosemic rats by aldose reductase or thromboxane synthetase inhibitors.
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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
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