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[EN] A study has been made of the effect of chronic exercise on myocardial electrophysiological heterogeneity and stability, as well as of the role of cholinergic neurons in these changes. Determinations in hearts from untrained and trained rabbits on a treadmill were performed. The hearts were isolated and perfused. A pacing electrode and a recording multielectrode were located in the left ventricle. The parameters determined during induced VF, before and after atropine (1 mu M), were: fibrillatory cycle length (VV), ventricular functional refractory period (FRPVF), normalized energy (NE) of the fibrillatory signal and its coefficient of variation (CV), and electrical ventricular activation complexity, as an approach to myocardial heterogeneity and stability. The VV interval was longer in the trained group than in the control group both prior to atropine (78 +/- 10 vs. 68 +/- 10 ms) and after atropine (76 +/- 8 vs. 67 +/- 10 ms). Likewise, FRPVF was longer in the trained group than in the control group both prior to and after atropine (53 +/- 8 vs. 42 +/- 7 ms and 50 +/- 6 vs. 40 +/- 6 ms, respectively), and atropine did not modify FRPVF. The CV of FRPVF was lower in the trained group than in the control group prior to atropine (12.5 +/- 1.5% vs. 15.1 +/- 3.8%) and, decreased after atropine (15.1 +/- 3.8% vs. 12.2 +/- 2.4%) in the control group. The trained group showed higher NE values before (0.40 +/- 0.04 vs. 0.36 +/- 0.05) and after atropine (0.37 +/- 0.04 vs. 0.34 +/- 0.06; p = 0.08). Training decreased the CV of NE both before (23.3 +/- 2% vs. 25.2 +/- 4%; p = 0.08) and after parasympathetic blockade (22.6 +/- 1% vs. 26.1 +/- 5%). Cholinergic blockade did not modify these parameters within the control and trained groups. Activation complexity was lower in the trained than in the control animals before atropine (34 +/- 8 vs. 41 +/- 5), and increased after atropine in the control group (41 +/- 5 vs. 48 +/- 9, respectively). Thus, training decreases the intrinsi

[EN] PurposeMechanical stretch increases sodium and calcium entry into myocytes and activates the late sodium current. GS967, a triazolopyridine derivative, is a sodium channel blocker with preferential effects on the late sodium current. The present study evaluates whether GS967 inhibits or modulates the arrhythmogenic electrophysiological effects of myocardial stretch.MethodsAtrial and ventricular refractoriness and ventricular fibrillation modifications induced by acute stretch were studied in Langendorff-perfused rabbit hearts (n=28) using epicardial multiple electrodes and high-resolution mapping techniques under control conditions and during the perfusion of GS967 at different concentrations (0.03, 0.1, and 0.3M).ResultsOn comparing ventricular refractoriness, conduction velocity and wavelength obtained before stretch had no significant changes under each GS967 concentration while atrial refractoriness increased under GS967 0.3M. Under GS967, the stretch-induced changes were attenuated, and no significant differences were observed between before and during stretch. GS967 0.3M diminished the normal stretch-induced changes resulting in longer (less shortened) atrial refractoriness (13826ms vs 95 +/- 9ms; p<0.01), ventricular refractoriness (155 +/- 18ms vs 124 +/- 16 ms; p<0.01) and increments in spectral concentration (23 +/- 5% vs 17 +/- 2%; p<0.01), the fifth percentile of ventricular activation intervals (46 +/- 8ms vs 31 +/- 3ms; p<0.05), and wavelength of ventricular fibrillation (2.5 +/- 0.5cm vs 1.7 +/- 0.3cm; p<0.05) during stretch. The stretch-induced increments in dominant frequency during ventricular fibrillation (control=38%, 0.03M=33%, 0.1M=33%, 0.3M=14%; p<0.01) and the stretch-induced increments in arrhythmia complexity index (control=62%, 0.03M=41%, 0.1M=32%, 0.3M=16%; p<0.05) progressively decreased on increasing the GS967 concentration.Conclusions GS967 attenuates stretch-induced changes in cardiac electrophysiology.

[EN] Electromechanical coupling studies have described the intervention of nitric oxide and S-nitrosylation processes in Ca2+ release induced by stretch, with heterogeneous findings. On the other hand, ion channel function activated by stretch is influenced by nitric oxide, and concentration-dependent biphasic effects upon several cellular functions have been described. The present study uses isolated and perfused rabbit hearts to investigate the changes in mechanoelectric feedback produced by two different concentrations of the nitric oxide carrier S-nitrosoglutathione. Epicardial multielectrodes were used to record myocardial activation at baseline and during and after left ventricular free wall stretch using an intraventricular device. Three experimental series were studied: (a) control (n=10); (b) S-nitrosoglutathione 10 mu M (n=11); and (c) S-nitrosoglutathione 50 mu M (n=11). The changes in ventricular fibrillation (VF) pattern induced by stretch were analyzed and compared. S-nitrosoglutathione 10 mu M did not modify VF at baseline, but attenuated acceleration of the arrhythmia (15.6 +/- 1.7 vs. 21.3 +/- 3.8Hz; p<0.0001) and reduction of percentile 5 of the activation intervals (42 +/- 3 vs. 38 +/- 4ms; p<0.05) induced by stretch. In contrast, at baseline using the 50 mu M concentration, percentile 5 was shortened (38 +/- 6 vs. 52 +/- 10ms; p<0.005) and the complexity index increased (1.77 +/- 0.18 vs. 1.27 +/- 0.13; p<0.0001). The greatest complexity indices (1.84 +/- 0.17; p<0.05) were obtained during stretch in this series. S-nitrosoglutathione 10 mu M attenuates the effects of mechanoelectric feedback, while at a concentration of 50 mu M the drug alters the baseline VF pattern and accentuates the increase in complexity of the arrhythmia induced by myocardial stretch.

Prussian blue (PB) represents a simple, economical, and eco‐friendly system as cathode material for sodium‐ion batteries (SIBs). However, structural problems usually worsen its experimental performance thus motivating the search for alternative synthetic strategies and the formation of composites that compensate these deficiencies. Herein, a straightforward approach for the preparation of PB/MoS2‐based nanocomposites is presented. MoS2 provides a 2D active support for the homogeneous nucleation of porous PB nanocrystals, which feature superior surface areas than those obtained by other methodologies, giving rise to a compact PB shell covering the full flake. The nanocomposite exhibits an excellent performance as cathode for SIBs with discharge capacity values up to 177 mA h g−1 and a specific capacitance of 354 F g−1. These values are even larger for the intercalation of K+ ions (up to 215 mA h g−1, reaching a specific capacitance of 489 F g−1). Compared to similar composites, superior performance can be ascribed to a synergistic effect of the coordination compound with the 2D material.