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1 Research Center, Montreal Heart Institute, Montreal, Canada
* To whom correspondence should be addressed. E-mail: stanley.nattel{at}icm-mhi.org.
Cardiac tissue in the pulmonary vein sleeves plays an important role in clinical atrial fibrillation. Mechanisms leading to pulmonary vein activity in atrial fibrillation remain unclear. Indirect experimental evidence points to pulmonary vein Ca2+-handling as a potential culprit, but there are no direct studies of pulmonary vein cardiomyocyte Ca2+-handling in the literature. We used the Ca2+-sensitive dye Indo-1-AM to study Ca2+-handling in isolated canine pulmonary vein and left atrial myocytes. Results were obtained at 35°C and room temperature in cells from control dogs, as well as in cardiomyocytes from dogs subjected to 7-day rapid atrial pacing. We found that basic Ca2+-transient properties (amplitude: 186±28 vs. 216±25 nM; stimulus to half-decay time: 192±9 vs. 192±9 ms; atria vs. pulmonary vein respectively at 1 Hz), beat-to-beat regularity, propensity to alternans, 
-adrenergic response (amplitude increase at 0.4 Hz: 96±52% vs. 129±61%), number of spontaneous Ca2+-transient events following Ca2+-loading (in normal Tyrode: 0.9±0.2 vs. 1.3±0.2; with 1 µM isoproterenol: 7.6±0.3 vs. 5.1±1.8 events per min), and caffeine-induced Ca2+-transient amplitudes were not significantly different between atrial and pulmonary vein cardiomyocytes. In an arrhythmia-promoting model (dogs subjected to 7-day atrial tachypacing), Ca2+-transient amplitude and kinetics were the same in cells from both pulmonary veins and atrium. In conclusion, the similar Ca2+-handling properties of canine pulmonary vein and left atrial cardiomyocytes that we observed do not support the hypothesis that intrinsic Ca2+-handling differences account for the role of pulmonary veins in atrial fibrillation.
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