Bulletin of the American Physical Society
2005 APS March Meeting
Monday–Friday, March 21–25, 2005; Los Angeles, CA
Session L21: Focus Session: Intracellular Calcium Dynamics in Myocytes |
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Sponsoring Units: DBP Chair: Wouter-Jan Rappel, UCSD Room: LACC 409A |
Tuesday, March 22, 2005 2:30PM - 3:06PM |
L21.00001: Intracellular Ca Cycling and ventricular fibrillation Invited Speaker: |
Tuesday, March 22, 2005 3:06PM - 3:18PM |
L21.00002: Investigating a Period-Doubling Bifurcation in Cardiac Tissue Using Alternate Pacing C.M. Berger, H.M. Dobrovolny, S.S. Kalb, S.F. Idriss, D.G. Schaeffer, D.J. Gauthier, W. Krassowska The action potential duration (APD) of cardiac cells undergoes a period-doubling bifurcation when the pacing rate (PR) is increased, resulting in a period-2 behavior called alternans. Studying the susceptibility of cardiac tissue to alternans is crucial because alternans can lead to ventricular fibrillation and sudden cardiac death. One way to study this behavior is to alternate the PR from beat-to-beat, which results in beat-to-beat alternation in APD. Recent mathematical models predict that these small beat-to-beat changes in PR will result in divergent beat-to-beat variations in APD near the period-doubling bifurcation. Thus, the appearance of divergent behavior during alternate pacing can uncover the tissue's propensity to alternans. In an experiment to test this hypothesis, we observed beat-to-beat APD variations that are only a fraction of the beat-to-beat change in the PR, despite proximity to the bifurcation point. This study demonstrates the discrepancy between experiment and theory, which may be due to changes in ionic concentrations and wave propagation. [Preview Abstract] |
Tuesday, March 22, 2005 3:18PM - 3:30PM |
L21.00003: Spatiotemporal dynamics and control of alternans in cardiac tissue with short-term memory Hana Dobrovolny, Elena Tolkacheva, Daniel Gauthier Alternans is an abnormal cardiac rhythm that is a precursor of fibrillation. Recently, an amplitude equation describing spatiotemporal dynamics of alternans in a one-dimensional cable [1] was derived using a model that assumes the current action potential duration (APD) depends on the previous diastolic interval (DI). However, experimental work has shown that cardiac tissue is more accurately described by models that contain some degree of ``memory,'' where the current APD depends on preceding APD's and DI's. We add memory to the amplitude equation and find that it adds a new parameter to the equation which governs the onset of alternans. We also find that memory affects the ability to control spatially concordant alternans, but has no effect on the ability to control discordant alternans. Analytical results are verified by simulations using the Fenton-Karma model. [1] B. Echebarria, A. Karma, \textit{Chaos}, \textbf{12}:923 (2002) [Preview Abstract] |
Tuesday, March 22, 2005 3:30PM - 4:06PM |
L21.00004: Excitation-contraction coupling gain and cooperativity of the cardiac ryanodine receptor: a modeling approach Invited Speaker: During calcium-induced-calcium-release, the ryanodine receptor opens and releases large amounts of calcium from the sarcoplasmic reticulum into the cytoplasm of the myocyte. Recent experiments have suggested that cooperativity between the four monomers comprising the ryanodine receptor plays an important role in the dynamics of the overall receptor. Furthermore, this cooperativity can be affected by the binding of FK506 binding protein and hence modulated by adrenergic stimulation through the phosphorylating action of PKA. This has important implications for heart failure, where it has been hypothesized that ryanodine receptor hyperphosphorylation, resulting in a loss of cooperativity, can lead to a persistent leak and a reduced sarcoplasmic reticulum content. Here, we report on a theoretical model that examines the cooperativity via the assumption of an allosteric interaction between the four subunits. We find that the level of cooperativity, regulated by the binding of FK506 binding protein, can have a dramatic effect on the excitation-contraction coupling gain and that this gain exhibits a clear maximum. These findings offer a simple explanation of heretofore conflicting data from different species and allows for an evaluation of the aforementioned heart failure scenario. [Preview Abstract] |
Tuesday, March 22, 2005 4:06PM - 4:18PM |
L21.00005: Antiphase calcium oscillations in astrocytes via inositol (1,4,5)-triphosphate regeneration. Ghanim Ullah, Peter Jung, Ann H. Cornell-Bell In cultured astrocytes, antiphase oscillations in the intracellular free calcium concentrations have been observed in nearest neighbor cells that are coupled through gap junctions. A mathematical model is used to investigate physiologic conditions under which diffusion of the second messenger inositol (1, 4, 5)-triphosphate (IP3) through gap junctions can facilitate synchronized antiphase calcium oscillations. Our model predicts antiphase oscillations in both calcium and IP3 concentrations if a) the gap junction permeability is within a window of values and 2) IP3 is regenerated in the astrocytes via Phospholipids-C$\delta $. This result sheds new light on the current dispute on the mechanism of intercellular calcium wave propagation since it provides additional evidence for a partially regenerative mechanism as the model excludes synchrony in the absence of IP3 regeneration. [Preview Abstract] |
Tuesday, March 22, 2005 4:18PM - 4:30PM |
L21.00006: Noise-induced ectopic activity in a simple cardiac cell model Harold Hastings, Alex Zaharakis, Christain Hilaire, Elizabeth Cherry, Flavio Fenton, Sabrina Sobel Ectopic activity in the form of premature ventricular contractions (PVCs) is relatively common in the normal heart. Although PVCs are normally harmless, sometimes but rarely PVCs can generate spiral waves of activation through interaction with other waves of activation, potentially progressing to ventricular tachycardia, followed by ventricular fibrillation and sudden cardiac death. Clusters of PVCs have been found to be significantly more dangerous than isolated PVCs. We model PVC generation by applying triggers (noise) to the generic FitzHugh-Nagumo model as substrate, and study the effects the noise level and excitability. We find: exponential waiting time behavior at fixed parameter levels; no evidence of clustering at fixed parameter levels; and a sharp increase in PVCs as excitability approaches the auto-oscillatory threshold or noise increases beyond a similar threshold. This produces sharp increases in theoretical rates of PVC-induced fibrillation, consistent with results of A Gelzer et al. in animal models. Partially supported by the NSF and NIH. [Preview Abstract] |
Tuesday, March 22, 2005 4:30PM - 4:42PM |
L21.00007: Diffusive transport through the myocardium of pharmacological agents placed in the pericardial space Xianfeng Song, Keith L. March, Sima Setayeshgar The classical understanding of the pericardial sac is as a fluid-filled space surrounding the heart. Since it is a self-contained space, it can be viewed as a reservoir and therapeutically used as a drug container to deliver agents to the myocardium. It is only recently that experimental techniques for safe delivery of agents to the pericardial space have been developed. In this work, we present a quantitative model of the key biophysical processes affecting the distribution through the myocardium of a substrate delivered to the pericardial sac. By direct analysis of experimental data on pericardial delivery of agents to the porcine heart and comparison with computational results, we determine quantitatively for the first time values for fundamental physical parameters, such as effective diffusion constant and washout rate, for small and large molecular weight test agents in the myocardium. We comment on the efficacy of this mode of drug delivery to the myocardium, thereby aiding in the development of agents and methods of delivery that achieve various therapeutic goals. [Preview Abstract] |
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L21.00008: Best Stiffness for Striation: Effect of Matrix Stiffness on Myocytes and Stem Cells Dennis Discher, Adam Engler Contractile myocytes provide a test of the hypothesis that cells sense their mechanical as well as molecular microenvironment, altering expression, organization, and/or morphology accordingly. Here, myoblasts and stem cells were cultured on collagen strips attached to glass or polymer gels of varied elasticity. MyoD expression and morphology peaks on gels with stiffness typical of normal muscle (passive Young's modulus $E \quad \sim $9-15 kPa). While fusion of myoblasts into myotubes occurs independent of substrate flexibility, myosin/ actin striations emerge later only on gels with the same tissue-like $E$. On glass and much softer or stiffer gels, including gels emulating stiff or fibrotic muscle, cells do not striate. In addition, myotubes grown on top of a compliant bottom layer of glass-attached myotubes (but not softer fibroblasts) will striate, whereas the bottom cells will only assemble stress fibers and vinculin-rich adhesions. Unlike sarcomere formation, adhesion strength increases monotonically versus substrate stiffness with strongest adhesion on glass. These findings have major implications for in vivo introduction of stem cells into diseased or damaged striated muscle of altered mechanical composition. [Preview Abstract] |
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