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The flux of thiamine from the blood into the brain has been measured using a specially devised technique by which a steady raised level of the vitamin, with or without radioactive labelling, can be achieved rapidly and maintained in the bloodstream. This is done by a continuous injection, given at a rate which is adjusted by a pre-determined programme so as to replace the tracer at the rate at which it has been found to leave the circulation in previous experiments. A further programme was worked out to maintain, in a similar manner by a separate injection, a steady raised level in the bloodstream of a chemical analogue of thiamine, 1-[(4-amino-2-propyl-5-pyrimidinyl)methyl]-2-picolinium chloride HCl (amprolium). In the presence of a high concentration of amprolium the flux of thiamine across the blood-brain barrier was greatly reduced and no longer saturable by raising the blood thiamine concentration up to at least 10 microM. It was concluded that this analogue of thiamine inhibited the saturable component of thiamine transport across the barrier but not the non-saturable component. In a further series of experiments, progressively higher levels of thiamine were maintained in the bloodstream and the influx of the vitamin across the blood-brain barrier was measured. From kinetic analysis of the results, it was clear that the affinity of amprolium for the transport carrier was of a similar magnitude to that of thiamine itself. That the inhibition was competitive was shown by the way in which it could be overcome if the level of thiamine in the blood plasma was raised sufficiently above the normal.