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Cardiomyocyte coupling may necessitate coronary coupling, according to computer simulation involving electrochemical signaling across narrow extracellular clefts between cardiomyocytes. We hypothesized that u03b21,u2013-mediated adhesion scaffolds trans-activating NaV1. 5 channels within narrow perinex clefts near gap junctions, facilitating ephaptic coupling. Perinexi's increased sodium current density was measured at the Smart patch clamp, relative to non-junctional locations. In myocyte monolayers, adp1 significantly increased perinexi in guinea pig ventricles, and selectively reduced perinexic INa, but not whole cell INa.
Source link: https://doi.org/10.7554/eLife.37610
This paper introduces a new thermoelectric model to investigate the heart's behavior in cooling conditions. A simplified Karma model with temperature dependence is used to describe the ion exchange dynamics on a mesoscopic scale, while the propagation of the action potential is controlled by a macroscopic equation. In addition to perfusion and heat metabolism, we call the Penne equation related to the mono-domain equation by using the Joule effect to describe the temperature distribution in the system. We investigate the influence of the nonlinear coupling tensor and arterial temperature on the system's thermal and electrical responses. When the temperature rises, the duration of the action potential decreases, and the Joule coupling tensor plays a key role in the propagation of the potential.
Source link: https://doi.org/10.1063/5.0076726
Patients suffering from end stage of chronic kidney disease often need haemodialysis to normalize the electrolyte levels. Moreover, cardiovascular disease is the leading cause of death in CKD patients. Using a computational model, we investigated the effects of an electrolyte shift on cardiac signals in order to determine CVD. Different extracellular sodium, calcium, and potassium levels were tested in CKD patients on a cellular level, with different extracellular sodium, calcium, and potassium concentrations as in CKD patients. Simulations with [Ca2+]o variants were also carried out on the ventricular ECG level, as well as a 12-lead ECG.
Source link: https://doi.org/10.1515/cdbme-2018-0061
The introduction of two alternative explanations of EAD origination with increasing amplitudes that do not require constant limit cycles in fast subsystems is the main point of this essay. We show that EAD patterns with increasing amplitudes may also develop as a result of a delayed subcritical Hopf bifurcation or uncertain manifold of a saddle focus fixed point in the full fast-slow model describing the action potential. Our research extends the list of possible dynamical EAD mechanisms and may contribute to the development of a registry of drug reactions in preclinical cardiotoxicity testing.
Source link: https://doi.org/10.1371/journal.pone.0151178
However, the effect of 4-HNE on cardiac electrophysiology has yet to be established. Using the whole-cell patch clamp technique, we investigated the effects of 4-HNE on several cardiac ion channels, including human ether-a-go-go-go-go-go-goo-related channels in the present study. Short-term exposure to 100 bcM 4-HNE, which mimics local conditions under oxidative stress, reduced the amplitudes of rapidly activating delayed rectifier K+ in guinea pig ventricular myocytes and HEK293T cells overexpressing hERG. After treatment with 4-HNE10L, a decrease in mature membrane hERG protein was shown by a decrease in mature membrane hERG protein after analysis with surface biotinylation. The 4-HNE10L-induced decrease in mature hERG, caused by proteasomal degradation inhibitors, such as bortezomib, was prevented by bortezomib, indicating a retrograde degradation of membrane hERG due to 4-HNE. 4-HNE100S and 4-HNE10L suppressed IhERG in the same manner as a whole, with functional inhibition and downregulation of membrane expression of hERG. The exposure of 4-HNE under pathological oxidative stress may raise the risk of proarrhythmic events as a result of APD prolongation.
Source link: https://doi.org/10.1016/j.redox.2018.08.018
Here is a concise three-dimensional summary of cardiac action potential characteristics in terms of the current source. The three-dimensional AP illustration makes it possible to accurately estimate membrane resistance during repolarization, which is a key factor in ventricular repolarization modulation. The novel AP representation is therefore a useful tool for both in vivo and in silico cardiac electrophysiological experiments.
Source link: https://doi.org/10.4081/jbr.2014.2134
To investigate systematically the connection between action potential duration dispersion and susceptibility to re-entry, we used a computerized model of cardiac tissue. Methods We made an example of a 60 mm 2 D sheet of cardiac ventricular tissue using the Luo-Rudy phase 1 model, with maximum conductance of the K+ channel gKmax set to 0. 004 mm -2. Conclusion When APD dispersion is increased by a larger spatial area of heterogeneity, greater electrophysiological heterogeneity, and slower cell-to-cell coupling, we found a close relationship between increased APD dispersion and re-entrant arrhythmias.
Source link: https://doi.org/10.1186/1475-925X-4-11
Heart disease in athletes is common among many kinds, which can be irreversible. In health and sports care literature, the recording of heart rate and ECG waveforms from such individuals by wireless sensor networks has been shown. The time of Cardiac Action Potential Propagation, however, would be a more determinative parameter for instant to instant shifts.
Cardiac cells are dependent on specific sarcolemmal ion transporters to ensure the proper intracellular pH control. Two distinct NBC isoforms have been outlined in the center of the story: the electroneutral NBCn1 and the electrogenic NBCe1. In an in vivo mouse model with overexpression of NBCe1, the aim of this study was to investigate the role of NBCe1 in heart electrophysiology and in heart hypertrophy. We found a decline in both APD and electrocardiogram QT interval as a result of cardiac activity, with cardiac rate being corrected for the first time by NBCe1 importance for heart electrical activity.
Source link: https://doi.org/10.3389/fcvm.2022.862118
Abnormal activity potential results, whether present in long or short QT syndromes, can cause life-threatening arrhythmias. Cardiomyocytes cultured in u2013 were transplanted to express the light-sensitive cationic channel channelrhodopsin-2 or the anionic-selective opsin, ACR2. The ability of spatiotemporally defined optogenetic protocols to alter AP properties and prevent arrhythmogenesis in the hiPSC-CMs cell/tissue models was tested by detailed patch-clamp, confocal-microscopy, and optical mapping studies. The ACR2's activation of effective APD shortening varied with illumination timing, light-induced ChR2 activation triggered rapid prolongation or shortening of AP durations, while ACR2 stimulation enabled rapid AP durations. Using optogenetic cross-field stimulation, We next developed a SQTS-CMs-u2013-based tissue model of reentrant-arrhythmias. An APD-modulating optogenetic protocol was later developed to extend APD of the propagating wavefront's APD, effectively preventing arrhythmogenesis in this case. This research reveals the promise of optogenetics in investigating repolarization abnormalities and discovering novel antiarrhythmic drugs.
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