Publications by authors named "Eric R Cheek"

Introduction: Termination of ventricular fibrillation by electric shocks is believed to be due to the direct activation of large tissue mass that may be caused by microscopic virtual electrodes formed at discontinuities in tissue structure. Here, microscopic shock-induced activation was measured optically in myocyte cultures; spatially averaged microscopic Vm measurements were compared with macroscopic measurements from left ventricular (LV) tissue.

Methods And Results: Experiments were performed in linear cell strands of different width (approximately 0.

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Changes in intracellular calcium concentration (DeltaCa(i)2+) induced by electrical shocks may play an important role in defibrillation, but high-resolution DeltaCa(i)2+ measurements in a multicellular cardiac tissue and their relationship to corresponding Vm changes (DeltaVm) are lacking. Here, we measured shock-induced DeltaCa(i)2+ and DeltaV(m) in geometrically defined myocyte cultures. Cell strands (width=0.

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Defibrillation shocks induce nonlinear changes of transmembrane potential (DeltaVm) that determine the outcome of defibrillation. As shown earlier, strong shocks applied during action potential plateau cause nonmonotonic negative DeltaVm, where an initial hyperpolarization is followed by Vm shift to a more positive level. The biphasic negative DeltaVm can be attributable to (1) an inward ionic current or (2) membrane electroporation.

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Background: It is believed that defibrillation is due to shock-induced changes of transmembrane potential (DeltaV(m)) in the bulk of ventricular myocardium (so-called virtual electrodes), but experimental proof of this hypothesis is absent. Here, intramural shock-induced DeltaV(m) were measured for the first time in isolated preparations of left ventricle (LV) by an optical mapping technique.

Methods And Results: LV preparations were excised from porcine hearts (n=9) and perfused through a coronary artery.

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Strong electrical shocks can induce arrhythmias, which might explain why shocks fail to defibrillate. In this work, the localization of arrhythmia source and the relationship with local changes of transmembrane potential (V(m)) were determined in geometrically defined cell cultures using optical mapping technique. Uniform-field shocks with strength (E) of 10 to 50 V/cm were applied across cell strands with width of 0.

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