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1 Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA
* To whom correspondence should be addressed. E-mail: karagueuzian{at}cshs.org.
The influence of threshold electrical currents (EC) during regular drive on pulmonary vein (PV) and atrial myocardial cell action potential duration (APD) is unknown. We determined the effects of EC on cellular APD of PV, atria and ventricles in isolated-perfused and superfused male rat hearts (Fisher344 strain & 3-4 month old) at 37°C (N=14). We determined APD changes caused by sub- and threshold EC synchronized with a distant pacing electrode and delivered nearby cells from which transmembrane action potentials were recorded with glass microelectrode. Progressive APD shortening (P<0.001) and membrane hyperpolarization (P<0.05) developed over a 20 sec interval in the PV and atrial cells when the EC was delivered at <2 mm but not at >4 mm from the microelectrode. No such effects were seen in ventricular muscle cells. APD fully recovered 25 s after the cessation of EC application. Premature stimuli applied during EC-induced shortening of the APD caused rapid repetitive PV and atrial activity lasting 2 to 5 beats. Atropine (2 µM, N=10) prevented while propranolol (2 µM, N=5) had no effect on EC-induced APD shortening or repetitive activity. We conclude that EC shortens the APD and hyperpolarizes the membrane by local release of acetylcholine and causes to steep repolarization gradient in the vicinity of the current source leading to repetitive activity in atrial and PV cells during premature stimulation.
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