TY - JOUR
T1 - Discontinuous cardiac conduction
T2 - Coupling real cells to model cells
AU - Wagner, Mary B.
AU - Wilders, Ronald
AU - Kumar, Rajiv
AU - Wang, Yang gan
AU - Joyner, Ronald W.
PY - 2000
Y1 - 2000
N2 - We have developed the "coupling clamp" technique in which an isolated cardiac myocyte is coupled to either another isolated myocyte or to a real-time simulation of a cardiac action potential (AP). This method precisely controls the coupling conductance, GC, between the cells. Additionally, the membrane properties of either cell can be altered. Thus a wide variety of questions regarding modulation of propagation can be tested. By coupling a guinea pig ventricular cell and a Luo-Rudy AP model over a range of GC, we found the critical value of GC required for propagation was increased by nifedipine (6.8±0.1 nS in control vs. 8.8±0.2 nS, p<0.0001) and decreased by isoproterenol (5.3±0.2 nS, p<0.001) (mean±SEM). Thus with less calcium current (ICa) available (blocked by nifedipine), more conductance was required for propagation. Additionally, with enhanced ICa (stimulation by isoproterenol) less conductance was required for propagation, thereby demonstrating the importance of ICa in maintaining propagation at low values of GC. We extended our coupling clamp technique to include the ability to couple a real cell to an array of 49 model cells. We coupled atrioventricular node cells to an array of either ventricular or atrial model cells and varied the size of the focus cell and the conductance of the array. For all GC tested, the critical size of the focus was smaller for activation of an atrial versus a ventricular array. The major differences between activation of the arrays are due to the higher membrane resistance (lower IK1) of the atrial versus ventricular cells.
AB - We have developed the "coupling clamp" technique in which an isolated cardiac myocyte is coupled to either another isolated myocyte or to a real-time simulation of a cardiac action potential (AP). This method precisely controls the coupling conductance, GC, between the cells. Additionally, the membrane properties of either cell can be altered. Thus a wide variety of questions regarding modulation of propagation can be tested. By coupling a guinea pig ventricular cell and a Luo-Rudy AP model over a range of GC, we found the critical value of GC required for propagation was increased by nifedipine (6.8±0.1 nS in control vs. 8.8±0.2 nS, p<0.0001) and decreased by isoproterenol (5.3±0.2 nS, p<0.001) (mean±SEM). Thus with less calcium current (ICa) available (blocked by nifedipine), more conductance was required for propagation. Additionally, with enhanced ICa (stimulation by isoproterenol) less conductance was required for propagation, thereby demonstrating the importance of ICa in maintaining propagation at low values of GC. We extended our coupling clamp technique to include the ability to couple a real cell to an array of 49 model cells. We coupled atrioventricular node cells to an array of either ventricular or atrial model cells and varied the size of the focus cell and the conductance of the array. For all GC tested, the critical size of the focus was smaller for activation of an atrial versus a ventricular array. The major differences between activation of the arrays are due to the higher membrane resistance (lower IK1) of the atrial versus ventricular cells.
KW - Coupling clamp
KW - Electrophysiology
KW - Propagation
UR - http://www.scopus.com/inward/record.url?scp=0034445289&partnerID=8YFLogxK
U2 - https://doi.org/10.1109/IEMBS.2000.900830
DO - https://doi.org/10.1109/IEMBS.2000.900830
M3 - Article
SN - 0589-1019
VL - 1
SP - 657
EP - 660
JO - Annual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings
JF - Annual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings
ER -