The research aim of the project is to study the mechanisms by which the spatial inhomogenities of membrane properties and cell-cell coupling determine the normal and abnormal activation sequence of the heart. The specific focus of this research is the junctional region between Purkinje (P) cells and the underlying Ventricular (V) endocardium. The techniques used include both numerical simulation of action potential propagation and experimental mapping of P and V activation sequences. The particular relevance of these studies is that the junctional region between P cells and V cells not only forms an essential part of the normal cardiac excitation sequence, but may also be involved in the abnormal excitation sequences produced under ischemic conditions. Our hypothesis is that the activation sequence is determined not only by differences in excitability between P cells and V cells, but also by particular spatial distribution of partial electrical uncoupling between the two cell layers.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
2R01HL022562-06A1
Application #
3336962
Study Section
Cardiovascular Study Section (CVA)
Project Start
1978-07-01
Project End
1987-12-31
Budget Start
1985-01-01
Budget End
1985-12-31
Support Year
6
Fiscal Year
1985
Total Cost
Indirect Cost
Name
University of Iowa
Department
Type
Schools of Medicine
DUNS #
041294109
City
Iowa City
State
IA
Country
United States
Zip Code
52242
Joyner, R W; Wang, Y G; Wilders, R et al. (2000) A spontaneously active focus drives a model atrial sheet more easily than a model ventricular sheet. Am J Physiol Heart Circ Physiol 279:H752-63
Wang, Y G; Kumar, R; Wagner, M B et al. (2000) Electrical interactions between a real ventricular cell and an anisotropic two-dimensional sheet of model cells. Am J Physiol Heart Circ Physiol 278:H452-60
Wagner, M B; Wang, Y G; Kumar, R et al. (2000) Measurements of calcium transients in ventricular cells during discontinuous action potential conduction. Am J Physiol Heart Circ Physiol 278:H444-51
Wilders, R; Wagner, M B; Golod, D A et al. (2000) Effects of anisotropy on the development of cardiac arrhythmias associated with focal activity. Pflugers Arch 441:301-12
Wang, Y G; Wagner, M B; Kumar, R et al. (2000) Fast pacing facilitates discontinuous action potential propagation between rabbit atrial cells. Am J Physiol Heart Circ Physiol 279:H2095-103
Wilders, R; Verheijck, E E; Joyner, R W et al. (1999) Effects of ischemia on discontinuous action potential conduction in hybrid pairs of ventricular cells. Circulation 99:1623-9
Wagner, M B; Namiki, T; Wilders, R et al. (1999) Electrical interactions among real cardiac cells and cell models in a linear strand. Am J Physiol 276:H391-400
Golod, D A; Kumar, R; Joyner, R W (1998) Determinants of action potential initiation in isolated rabbit atrial and ventricular myocytes. Am J Physiol 274:H1902-13
Joyner, R W; Kumar, R; Golod, D A et al. (1998) Electrical interactions between a rabbit atrial cell and a nodal cell model. Am J Physiol 274:H2152-62
Verheijck, E E; Wilders, R; Joyner, R W et al. (1998) Pacemaker synchronization of electrically coupled rabbit sinoatrial node cells. J Gen Physiol 111:95-112

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