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Am J Physiol Heart Circ Physiol (October 11, 2001). doi:10.1152/ajpheart.00240.2001
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Articles in PresS, published online ahead of print October 11, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00240.2001
Submitted on March 26, 2001
Accepted on October 10, 2001

A possible role for atrial fibroblasts in post-infarction bradycardia

Andre Kamkin1, Irina Kiseleva1, Kay-Dietrich Wagner2*, Alexander Pylaev2, Kate P Leiterer3, Heinz Theres3, Holger Scholz2, Joachim Gunther2, and Gerrit Isenberg4

1 Institute of Physiology, Humboldt University, Charite, Berlin, Germany; Department of Physiology, Martin Luther University of Halle, Halle/Saale, Germany
2 Institute of Physiology, Humboldt University, Charite, Berlin, Germany
3 Clinic of Internal Medicine 1, Humboldt University, Charite, Berlin, Germany
4 Department of Physiology, Martin Luther University of Halle, Halle/Saale, Germany

* To whom correspondence should be addressed. E-mail: kay-dietrich.wagner{at}charite.de.

Atrial fibroblasts are considered to modulate the contractile activity of the heart in response to mechanical stretch. In this study we examined whether atrial fibroblasts are possibly involved in bradyarrhythmia, which is a severe complication after myocardial infarction. For this purpose, transmembrane electrical potentials were recorded in cardiac fibroblasts near the sino-atrial node from sham-operated rats and from rats with myocardial infarction. Twenty days after infarction due to coronary artery ligation, the right atrial tissue weights and the sensitivity of the fibroblast membrane potential to mechanical stretch correlated positively with the infarct size. Cardiac growth was enhanced but the stretch sensitivity and the resting membrane potential of the atrial fibroblasts declined between 8 and 30 days after infarction. The frequency of spontaneous atrial contractions was significantly reduced 8 days after myocardial infarction and recovered in parallel with the membrane potential of the fibroblasts. These findings suggest that changes in the susceptibility of atrial fibroblasts to mechanical stretch may contribute to bradyarrhythmia during post-infarct remodeling of the heart.




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