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This Article Full Text Full Text (PDF) All Versions of this Article: 293/1/H394    most recent 00833.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Oliveira, F. A. Articles by Cruz, J. S. Search for Related Content PubMed PubMed Citation Articles by Oliveira, F. A. Articles by Cruz, J. S.

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

Departments of ¹Biochemistry and Immunology and ²Physiology 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 Ca²⁺ 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 Ca²⁺ current density. Inactivation kinetics of this current in Ca²⁺-buffered cells was retarded in thiamine-deficient cardiac myocytes. The global Ca²⁺ release was significantly reduced in thiamine-deficient cardiac myocytes. The amplitude of caffeine-releasable Ca²⁺ 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 Ca²⁺ release.

arrhythmia; calcium current; confocal microscopy