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European Journal of Heart Failure Advance Access originally published online on October 29, 2009
European Journal of Heart Failure 2009 11(12):1126-1128; doi:10.1093/eurjhf/hfp146
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Impaired cellular contractile function in thiamine-deficient rat cardiomyocytes

Carolina Rosa Gioda1,2, Danilo Roman-Campos1, Miguel Araújo Carneiro-Júnior3, Karina Ana da Silva3, Matheus Ornelas de Souza3, Liliane Jorge Mendes1, Antônio José Natali3 and Jader Santos Cruz1,*

1 Laboratory of Excitable Membranes and Cardiovascular Biology, Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil
2 Biological Sciences Institute, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil
3 Department of Physical Education, Federal University of Viçosa, Viçosa, MG, Brazil

* Corresponding author. Tel: +55 31 3409 2668, Email: jcruz@icb.ufmg.br

Received April 22, 2009; Revised August 12, 2009; Accepted September 9, 2009

The first 10% of the full text of this article appears below.


   Background
 
Thiamine (vitamin B1) is an essential cofactor of important metabolic enzymes.1,2 Studies have demonstrated that thiamine deficiency (TD) leads to changes in cardiac morphological, electrophysiological and mechanical properties, as well as in cardiac metabolism.3–9 Clinical studies have indicated that the use of loop diuretics can induce TD and eventually cause heart dysfunction. The most important reported clinical manifestation of TD involves high-output heart failure. In humans, TD damages the cardiovascular system causing heart failure.10–12

The altered excitation-contraction coupling that characterizes cardiac failure occurs due to changes in Ca2+ dynamics, action potential duration, global Ca2+ transient, and contraction and relaxation rates.13 Oliveira et al.8 found that thiamine deprivation decreased the global Ca2+ release from the sarcoplasmic reticulum (SR) due to the lower SR Ca2+ load without changes in Ca2+ current density.


   Aim
 
. . . [Full Text of this Article]


   Methods
 
Cell isolation
Measurement of cellular contractility
Statistical analysis

   Results
 

   Conclusions
 

   Funding
 

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