Abstract
THE basic physiological mechanism affected by morphine may be that of the enzymatic processes involved in glucose metabolism: it is known, indeed, that morphine inhibits glucose and pyruvic acid utilization by minced brain1, and the decarboxylation by rabbit's liver and brain homogenates of pyruvic acid2. Further, morphine is known to reduce the level of carbon-14 in brains of rats fed with labelled glucose3. Cocarboxylase activity is unaffected in chronically morphinized rats, but responses to pyruvate and Cocarboxylase of in vitro muscle from animals deficient in thiamine and from chronically morphinized ones are similar, suggesting a metabolic defect in common to both conditions4; thiamine has no effect on morphine withdrawal symptoms in man5, though it decreases their intensity in rats6. Lastly, glycids and their metabolites change the analgesic effect of morphine.
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ANGELUCCI, L. Influence of Cocarboxylase on Tolerance to Morphine in the Rat. Nature 181, 967–968 (1958). https://doi.org/10.1038/181967a0
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DOI: https://doi.org/10.1038/181967a0
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