High resolution optical mapping of cardiac action potentials in freely beating rabbit hearts

Author(s):  
M. Inagaki ◽  
I. Hidaka ◽  
T. Aiba ◽  
T. Tatewaki ◽  
K. Sunagawa ◽  
...  
2006 ◽  
Vol 290 (3) ◽  
pp. H1298-H1306 ◽  
Author(s):  
William R. Mills ◽  
Niladri Mal ◽  
Farhad Forudi ◽  
Zoran B. Popovic ◽  
Marc S. Penn ◽  
...  

Late myocardial infarction (MI) is associated with ventricular arrhythmias and sudden cardiac death. The exact mechanistic relationship between abnormal cellular electrophysiology, conduction abnormalities, and arrhythmogenesis associated with late MI is not completely understood. We report a novel, rapid dye superfusion technique to enable whole heart, high-resolution optical mapping of late MI. Optical mapping of action potentials was performed in normal rats and rats with anterior MI 7 days after left anterior descending artery ligation. Hearts from normal rats exhibited normal action potentials and impulse conduction. With the use of programmed stimulation to assess arrhythmia inducibility, 29% of hearts with late MI had inducible sustained ventricular tachycardia, compared with 0% in normal rats. A causal relationship between the site of infarction, abnormal action potential conduction (i.e., block and slow conduction), and arrhythmogenesis was observed. Optical mapping techniques can be used to measure high-resolution action potentials in a whole heart model of late MI. This experimental model reproduces many of the electrophysiological characteristics (i.e., conduction slowing, block, and ventricular tachycardia) associated with MI in patients. Importantly, the results of this study can enhance our ability to understand the interplay between cellular heterogeneity, conduction abnormalities, and arrhythmogenesis associated with MI.


1988 ◽  
Vol 20 (2) ◽  
pp. 151-160 ◽  
Author(s):  
Robert King ◽  
Joyce Catlow ◽  
Michael Gwilt ◽  
Alan Higgins

2014 ◽  
Vol 4 (1) ◽  
Author(s):  
Sarah A. Park ◽  
Shin-Rong Lee ◽  
Leslie Tung ◽  
David T. Yue

2011 ◽  
Vol 58 (7) ◽  
pp. 2120-2126 ◽  
Author(s):  
Andrew D. Bachtel ◽  
Richard A. Gray ◽  
Jayna M. Stohlman ◽  
Elliot B. Bourgeois ◽  
Andrew E. Pollard ◽  
...  

2018 ◽  
Author(s):  
Steven Boggess ◽  
Shivaani Gandhi ◽  
Brian Siemons ◽  
Nathaniel Huebsch ◽  
Kevin Healy ◽  
...  

<div> <p>The ability to non-invasively monitor membrane potential dynamics in excitable cells like neurons and cardiomyocytes promises to revolutionize our understanding of the physiology and pathology of the brain and heart. Here, we report the design, synthesis, and application of a new class of fluorescent voltage indicator that makes use of a fluorene-based molecular wire as a voltage sensing domain to provide fast and sensitive measurements of membrane potential in both mammalian neurons and human-derived cardiomyocytes. We show that the best of the new probes, fluorene VoltageFluor 2 (fVF 2) readily reports on action potentials in mammalian neurons, detects perturbations to cardiac action potential waveform in human induced pluripotent stem cell (hiPSC)-derived cardiomyocytes, shows a substantial decrease in phototoxicity compared to existing molecular wire-based indicators, and can monitor cardiac action potentials for extended periods of time. Together, our results demonstrate the generalizability of a molecular wire approach to voltage sensing and highlights the utility of fVF 2 for interrogating membrane potential dynamics.</p> </div>


2021 ◽  
Author(s):  
José Guilherme Chaui-Berlinck ◽  
Vitor Rodrigues da Silva

Author(s):  
Maria P. Hortigon-Vinagre ◽  
Victor Zamora ◽  
Gary Gintant ◽  
Jonathon Green ◽  
Francis L. Burton ◽  
...  

2017 ◽  
Vol 114 (35) ◽  
pp. E7367-E7376 ◽  
Author(s):  
Rene Barro-Soria ◽  
Rosamary Ramentol ◽  
Sara I. Liin ◽  
Marta E. Perez ◽  
Robert S. Kass ◽  
...  

KCNE β-subunits assemble with and modulate the properties of voltage-gated K+ channels. In the heart, KCNE1 associates with the α-subunit KCNQ1 to generate the slowly activating, voltage-dependent potassium current (IKs) in the heart that controls the repolarization phase of cardiac action potentials. By contrast, in epithelial cells from the colon, stomach, and kidney, KCNE3 coassembles with KCNQ1 to form K+ channels that are voltage-independent K+ channels in the physiological voltage range and important for controlling water and salt secretion and absorption. How KCNE1 and KCNE3 subunits modify KCNQ1 channel gating so differently is largely unknown. Here, we use voltage clamp fluorometry to determine how KCNE1 and KCNE3 affect the voltage sensor and the gate of KCNQ1. By separating S4 movement and gate opening by mutations or phosphatidylinositol 4,5-bisphosphate depletion, we show that KCNE1 affects both the S4 movement and the gate, whereas KCNE3 affects the S4 movement and only affects the gate in KCNQ1 if an intact S4-to-gate coupling is present. Further, we show that a triple mutation in the middle of the transmembrane (TM) segment of KCNE3 introduces KCNE1-like effects on the second S4 movement and the gate. In addition, we show that differences in two residues at the external end of the KCNE TM segments underlie differences in the effects of the different KCNEs on the first S4 movement and the voltage sensor-to-gate coupling.


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