Planar microelectrode-cavity array for high-resolution and parallel electrical recording of membrane ionic currents

Lab on a Chip ◽  
2008 ◽  
Vol 8 (6) ◽  
pp. 938 ◽  
Author(s):  
Gerhard Baaken ◽  
Markus Sondermann ◽  
Christian Schlemmer ◽  
Jürgen Rühe ◽  
Jan C. Behrends
2002 ◽  
Vol 4 (3) ◽  
pp. 167-181 ◽  
Author(s):  
Simona Sanfelici

The aim of this work is twofold. First we focus on the complex phenomenon of electrogram fractionation, due to the presence of discontinuities in the conduction properties of the cardiac tissue in a bidomain model. Numerical simulations of paced activation may help to understand the role of the membrane ionic currents and of the changes in cellular coupling in the formation of conduction blocks and fractionation of the electrogram waveform. In particular, we show that fractionation is independent ofINAalterations and that it can be described by the bidomain model of cardiac tissue. Moreover, some deflections in fractionated electrograms may give nonlocal information about the shape of damaged areas, also revealing the presence of inhomogeneities in the intracellular conductivity of the medium at a distance.The second point of interest is the analysis of the effects of space–time discretization on numerical results, especially during slow conduction in damaged cardiac tissue. Indeed, large discretization steps can induce numerical artifacts such as slowing down of conduction velocity, alteration in extracellular and transmembrane potential waveforms or conduction blocks, which are not predicted by the continuous bidomain model. Several possible numerical and physiological explanations of these effects are given. Essentially, the discrete system obtained at the end of the approximation process may be interpreted as a discrete model of the cardiac tissue made up of isopotential cells where the effective intracellular conductivity tensor depends on the space discretization steps; the increase of these steps results in an increase of the effective intracellular resistance and can induce conduction blocks if a certain critical value is exceeded.


1999 ◽  
Vol 07 (04) ◽  
pp. 451-473 ◽  
Author(s):  
ALAIN VINET

Unidirectional propagation has been studied in a one-dimensional loop of model cardiac cells represented as a homogeneous and isotropic cable. Membrane ionic currents were represented by a modified Beeler-Reuter model. The time constants of the gate variables of the slow inward current acting during the plateau of the action potential were divided by a parameter K ≥1. In the space-clamped model, increasing K shortens the action potential duration, changes the shape of the restitution curve and adds a slow memory component to the dynamics. In a paced regime, it promotes bistability in which period-1 and period-2 patterns coexist over an interval of pacing frequencies. In the loop, bistability is created between periodic and aperiodic modes of sustained reentry for an interval of loop length. The bistability of the space-clamped and loop model are both related to the form of the restitution curve.


1995 ◽  
Vol 82 (2) ◽  
pp. 559-565 ◽  
Author(s):  
Noboru Hatakeyama ◽  
Yasunori Momose ◽  
Yusuke Ito

Background The effects of sevoflurane was examined on the contractile response, membrane potential, membrane ionic currents, and intracellular cyclic adenosine monophosphate (cAMP) in canine single ventricular myocytes. Methods Contraction was measured by a video-edge detector, and membrane ionic currents were recorded using whole-cell voltage clamp technique. Intracellular cAMP was measured with radioimmunoassay method. Results Sevoflurane (1.0-4.0%) decreased the contraction of single ventricular cells in a dose-dependent and reversible manner. Also, sevoflurane decreased the action potential plateau and shortened the duration of action potential. Sevoflurane reduced the peak Ca2+ currents (ICa) but did not show the use-dependent block. On the other hand, sevoflurane slightly reduced the Na+ currents (INa) only at a high concentration (4.0%). Intracellular cAMP concentration was reduced only at 4.0% sevoflurane. Conclusions The negative inotropic effect of sevoflurane is mediated via the inhibition of ICa in canine ventricular myocyte but not associated with reduced intracellular cAMP except at a high dose (4.0%).


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