Properties of thiamine transport in isolated perfused hearts of chronically alcoholic guinea pigs

The aim of this study was to determine the mechanism of transport of (14)C-thiamine in the hearts of healthy (nonalcoholic) and chronically alcoholic guinea pigs. We used the single-pass, paired-tracer dilution method on isolated and retrogradely perfused guinea pig hearts. The maximal cellular upta...

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Bibliographic Details
Published in:Canadian journal of physiology and pharmacology 2008-04, Vol.86 (4), p.160
Main Authors: Petrovic, Milos M, Scepanovic, Ljiljana, Rosic, Gvozden, Mitrovic, Dusan M
Format: Article
Language:English
Subjects:
Alcoholism - metabolism
Animals
Biological Transport, Active
Carbon Radioisotopes
Carbonyl Cyanide m-Chlorophenyl Hydrazone - pharmacology
Disease Models, Animal
Enzyme Inhibitors - pharmacology
Female
Guinea Pigs
Kinetics
Male
Myocardium - enzymology
Myocardium - metabolism
Ouabain - pharmacology
Oxidative Phosphorylation - drug effects
Perfusion
Radioisotope Dilution Technique
Sodium - metabolism
Sodium-Potassium-Exchanging ATPase - antagonists & inhibitors
Sodium-Potassium-Exchanging ATPase - metabolism
Thiamine - metabolism
Uncoupling Agents - pharmacology
Vitamin B Complex - metabolism
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Summary:The aim of this study was to determine the mechanism of transport of (14)C-thiamine in the hearts of healthy (nonalcoholic) and chronically alcoholic guinea pigs. We used the single-pass, paired-tracer dilution method on isolated and retrogradely perfused guinea pig hearts. The maximal cellular uptake (U(max)) and total cellular uptake (U(tot)) of (14)C-thiamine were determined under control conditions and under influence of possible modifiers. We tested how the presence of unlabeled thiamine, metabolic inhibitors, or absence of sodium ions influence the transport of (14)C-thiamine. The results of our experiments show that the transport of (14)C-thiamine is specific and energy-dependent and that its properties are significantly changed under the influence of chronic alcoholism. The latter effect occurs by increase in both U(max) and U(tot), as a manifestation of a compensatory mechanism in thiamine deficiency.
ISSN:0008-4212
DOI:10.1139/Y08-013