Related Experiment Video
Updated: Aug 9, 2026
Imaging Ca2+ Signals in Small Pulmonary Veins at Physiological Intraluminal Pressures
Published on: March 21, 2025
Sodium-calcium exchange initiated by the Ca2+ transient: an arrhythmia trigger within pulmonary veins
Eugene Patterson1, Ralph Lazzara, Bela Szabo
1University of Oklahoma Health Sciences Center and the DVA Medical Center, Oklahoma City, Oklahoma, USA. eugene-patterson@ouhsc.edu
Objectives:
The hypothesis that an increased or prolonged Ca2+ transient during an abbreviated action potential can give rise to early afterdepolarizations (EADs) and triggered arrhythmia by enhanced forward sodium-calcium (Na-Ca) exchange was examined.
Background:
Because pulmonary veins have the shortest action potential of any cardiac tissue, we examined this hypothesis in canine pulmonary vein sleeves during interventions further shortening the action potential and increasing the calcium transient.
Methods:
Extracellular bipolar electrode, intracellular microelectrode, and isometric force (a surrogate marker for the Ca2+ transient) recordings were obtained from superfused canine pulmonary veins.
Results:
An elevation and prolongation of the terminal phase of repolarization (EADs) were observed during interventions increasing contractile force; isoproterenol or norepinephrine (3.2 x 10(-11) to 3.2 x 10(-7)M), hypothermia, and pacing (post-extrasystolic potentiation, post-pacing pause). The EAD formation was prevented by ryanodine (10 microM) or reversed by transiently increasing [Ca2+](o) from 1.35 to 5 mM (inhibition of forward Na-Ca exchange). Pacing-induced EADs were enhanced by re-introduction of normal Tyrode solution (Na+ = 130 mM) after substitution of 30 mM NaCl with 30 mM LiCl (stimulation of forward Na-Ca exchange). With norepinephrine or isoproterenol (3.2 x 10(-8)M) + acetylcholine (10(-7)M) (to enhance the Ca2+ transient and further shorten the abbreviated action potential, respectively), tachycardia-pause initiated arrhythmia (1,132 +/- 153 beats/min) lasting >1 s was observed. Rapid firing was prevented by either suppression of the Ca2+ transient (ryanodine) or transiently increasing [Ca2+](o).
Conclusions:
The data show EAD formation in superfused canine pulmonary veins, enhanced by an increased Ca2+ transient and increased Na-Ca exchange current. With subsequent shortening of the action potential with acetylcholine, tachycardia-pause triggers rapid firing within the PV sleeve.
More Related Videos
Related Concept Videos
01:19Electrophysiology of Normal Cardiac Rhythm
01:27Feedback Regulation of Calcium Concentration
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
01:28Mechanism of Cardiac Arrhythmias
01:13The Cardiac Cycle
The Process
Electrical signals—sent from the sinoatrial (SA) node in the right atrial wall to the atrioventricular (AV) node between the right atrium and right ventricle—cause both atria to simultaneously contract. When the signal reaches the AV node, it pauses for approximately a tenth of a second, allowing the atria to contract and empty blood into the...
01:30Cardiac Action Potential
The cardiac action potential process involves a series of phases characterized by the movement of ions across the cardiac cell membranes, leading to the depolarization and repolarization of the cardiac myocytes.
Ionic Basis of Cardiac Action Potentials
01:25ECG Interpretation of Arrhythmias II: Atrial, Junctional and Ventricular Arrhythmias