Blood-brain barrier dysfunction in thiamine-deficient, alcohol-treated rats.

Rats maintained on a thiamine-deficient diet for 38 days loss weight and showed neurological symptoms. The PA value, representing the permeability of the blood-brain barrier to 14C-sucrose, was significantly increased whether urethane or ethanol was used as anaesthetic. This increase was prevented by giving rats on the same diet injections of thiamine twice weekly. Barrier function was normalised by injecting thiamine into deficient rats for just 3 days before biopsy. The brains of the thiamine-deficient rats were stained by the Fink-Heimer method but showed no degenerating axons except for silver grains in the glomeruli of the olfactory bulb. Other rats were maintained on the same diet for 38 days and additionally exposed to ethanol vapour for 16 h per day. This resulted in a similar loss of weight but a greater leakage of the blood-brain barrier. The latter was normalised by a thiamine injection only 24 h before biopsy, but was not reduced by withdrawal of ethanol for 3 days before biopsy. Axonal degeneration was present in the olfactory glomeruli. However, no lesions or extravasated blood cells were seen in any brains, there was no change in brain water indicative of oedema and no degeneration in retina, distal peripheral nerves or leg muscles. The relation of these and other experimental findings to alcohol-related brain damage is considered.