Abolition of reperfusion-induced arrhythmias in hearts from thiamine-deficient rats

Departments of 1 Biochemistry and Immunology and 2 Physiology and Biophysics, Biological Sciences Institute, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil Submitted 2 August 2006 ; accepted in final form 8 March 2007 Extensive work has been done regarding the impact of thiamine depriv...

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Veröffentlicht in:American journal of physiology. Heart and circulatory physiology 2007-07, Vol.293 (1), p.H394-H401
Hauptverfasser: Oliveira, Fernando A, Guatimosim, Silvia, Castro, Carlos H, Galan, Diogo T, Lauton-Santos, Sandra, Ribeiro, Angela M, Almeida, Alvair P, Cruz, Jader S
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Sprache:eng
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Zusammenfassung:Departments of 1 Biochemistry and Immunology and 2 Physiology and Biophysics, Biological Sciences Institute, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil Submitted 2 August 2006 ; accepted in final form 8 March 2007 Extensive work has been done regarding the impact of thiamine deprivation on the nervous system. In cardiac tissue, chronic thiamine deficiency is described to cause changes in the myocardium that can be associated with arrhythmias. However, compared with the brain, very little is known about the effects of thiamine deficiency on the heart. Thus this study was undertaken to explore whether thiamine deprivation has a role in cardiac arrhythmogenesis. We examined hearts isolated from thiamine-deprived and control rats. We measured heart rate, diastolic and systolic tension, and contraction and relaxation rates. Whole cell voltage clamp was performed in rat isolated cardiac myocytes to measure L-type Ca 2+ current. In addition, we investigated the global intracellular calcium transients by using confocal microscopy in the line-scan mode. The hearts from thiamine-deficient rats did not degenerate into ventricular fibrillation during 30 min of reperfusion after 15 min of coronary occlusion. The antiarrhythmogenic effects were characterized by the arrhythmia severity index. Our results suggest that hearts from thiamine-deficient rats did not experience irreversible arrhythmias. There was no change in L-type Ca 2+ current density. Inactivation kinetics of this current in Ca 2+ -buffered cells was retarded in thiamine-deficient cardiac myocytes. The global Ca 2+ release was significantly reduced in thiamine-deficient cardiac myocytes. The amplitude of caffeine-releasable Ca 2+ was lower in thiamine-deficient myocytes. In summary, we have found that thiamine deprivation attenuates the incidence and severity of postischemic arrhythmias, possibly through a mechanism involving a decrease in global Ca 2+ release. arrhythmia; calcium current; confocal microscopy Address for reprint requests and other correspondence: J. S. Cruz, Dept. of Biochemistry and Immunology, Universidade Federal de Minas Gerais, Belo Horizonte, MG, CEP 31900-901, Brazil (e-mail: jcruz{at}icb.ufmg.br )
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.00833.2006