Energetic metabolism during acute stretch-related atrial fibrillation

Background and methods Perturbations in energetic metabolism and impaired atrial contractility may play an important role in the pathogenesis of atrial fibrillation (AF). Besides, atrial stretch is commonly associated with AF. However, the atrial energetics of stretch-related AF are poorly understoo...

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Veröffentlicht in:Molecular and cellular biochemistry 2008-10, Vol.317 (1-2), p.69-75
Hauptverfasser: Kalifa, Jérôme, Maixent, Jean-Michel, Chalvidan, Thierry, Dalmasso, Christiane, Colin, David, Cozma, Dragos, Laurent, Pierre, Deharo, Jean-Claude, Djiane, Pierre, Cozzone, Patrick, Bernard, Monique
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Sprache:eng
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Zusammenfassung:Background and methods Perturbations in energetic metabolism and impaired atrial contractility may play an important role in the pathogenesis of atrial fibrillation (AF). Besides, atrial stretch is commonly associated with AF. However, the atrial energetics of stretch-related AF are poorly understood. Here, we measured indicators of energy metabolism during acute stretch-related AF. PCr, adenine nucleotides, and derivatives concentrations as well as the activity of the F 0 F 1 -ATPase and Na,K-ATPase were obtained after 1 h of stretch and/or AF in isolated rabbit hearts and compared to control hearts without stretch and AF. Results After 1 h of stretch-related AF, the total adenine nucleotides’ pool was significantly lower (42.2 ± 2.6 vs. 63.7 ± 8.3 μmol/g protein in control group, P < 0.05) and the PCr/ATP ratio significantly higher (2.3 ± 0.3 vs. 1.1 ± 0.1 in control group P < 0.05), because of ATP, ADP, and AMP decrease and PCr increase. The sum of high-energy phosphate compounds did not change. There were no significant differences in F 0 F 1 -ATPase nor Na,K-ATPase activity between the groups. Conclusions Results show that in this experimental model, acute stretch-related AF induces specific modifications of atrial myocytes energetics that may play a pivotal role in the perpetuation of the arrhythmia.
ISSN:0300-8177
1573-4919
DOI:10.1007/s11010-008-9832-3