6-lead surface electrocardiogram (ecg)  (ADInstruments)

Journal: Physiological Reports

Article Title: Uremia increases QRS duration after β ‐adrenergic stimulation in mice

doi: 10.14814/phy2.13720

Figure Lengend Snippet: (A) Male mice were subjected to 5/6 nephrectomy ( NX ) or sham operation. A period of 8–9 weeks later, echocardiography, ECG telemetry, cardiac pacing, and conduction‐velocity measurements were performed on the indicated number of mice. Some, but not all mice were used for more than one test. (B) Plasma markers of kidney function, urea, and creatinine, were measured in plasma samples taken from NX (black circles) and sham‐operated (white circles) mice at the termination of the study. * P < 0.05 (Student's t test).

Article Snippet: Mice were anesthetized using 2% isoflurane in a mix of O 2 and N 2 (30:70) and a standard 6‐lead surface ECG was recorded for 10 min before any surgery (LabChart, ADInstruments, Australia).

Techniques: Clinical Proteomics

Journal: Physiological Reports

Article Title: Uremia increases QRS duration after β ‐adrenergic stimulation in mice

doi: 10.14814/phy2.13720

Figure Lengend Snippet: (A) Representative ECG traces from conscious NX and sham mice. P wave, QRS complex, and T wave are indicated on the first complex. (B) RR intervals during 24 h in NX and sham mice. The light was on from 6 am to 6 pm (0–12 h on the abscissa, indicated by a white box) and off from 6 pm to 6 am (12–24 h on the abscissa, indicated by a black box). The indicated fits are from a three‐parameter cosinor function with a fixed phase of 24 h. We tested the probability of an amplitude of zero (i.e. , no 24‐h rhythm), and plotted the fit only if P < 0.05. The amplitude of the fit, i.e., from mean to peak, is indicated on the graph. * P < 0.05 versus the amplitude of the NX fit. (C) QRS intervals during 24 h. Details as in panel B. There was no 24‐h rhythm of QRS complexes in NX mice. (D) QT intervals during 24 h. Details as in panel B.

Article Snippet: Mice were anesthetized using 2% isoflurane in a mix of O 2 and N 2 (30:70) and a standard 6‐lead surface ECG was recorded for 10 min before any surgery (LabChart, ADInstruments, Australia).

Techniques: IF-P

Journal: Physiological Reports

Article Title: Uremia increases QRS duration after β ‐adrenergic stimulation in mice

doi: 10.14814/phy2.13720

Figure Lengend Snippet: (A) RR intervals measured every minute before and after isoprenaline administration in conscious mice. (B) QRS intervals measured every minute before and after isoprenaline administration in conscious mice. * indicates a statistically significant difference between NX and sham‐operated mice based on a two‐way ANOVA on all postadministration data points. (C) Representative ECG traces from conscious NX and sham‐operated mice, before and after isoprenaline administration. Note the change in QRS morphology after isoprenaline in the NX mice, causing an overall prolongation of the QRS duration.

Article Snippet: Mice were anesthetized using 2% isoflurane in a mix of O 2 and N 2 (30:70) and a standard 6‐lead surface ECG was recorded for 10 min before any surgery (LabChart, ADInstruments, Australia).

Techniques:

Journal: Physiological Reports

Article Title: Uremia increases QRS duration after β ‐adrenergic stimulation in mice

doi: 10.14814/phy2.13720

Figure Lengend Snippet: (A) Representative surface electrocardiograms ( ECG ) and intracardiac electrogram ( EGM ) from an NX and a control mice. Stimulus (stim) indicates right ventricular apex pacing. Mice were paced before and after administration of isoprenaline. Arrow points to the His potential on the EGM . (B) QRS duration in NX and control mice during normal sinus rhythm (no pacing) and during ventricular pacing, before and after administration of isoprenaline. Ventricular pacing causes a twofold prolongation of the QRS interval that was comparable in both mice groups. There is a trend toward a statistically significant isoprenaline‐induced prolongation of the QRS complex in NX mice ( P = 0.06), but not in sham‐operated mice ( P = 0.50).

Article Snippet: Mice were anesthetized using 2% isoflurane in a mix of O 2 and N 2 (30:70) and a standard 6‐lead surface ECG was recorded for 10 min before any surgery (LabChart, ADInstruments, Australia).

Techniques: Control

Journal: Scientific Reports

Article Title: Overexpression of Cx43 in cells of the myocardial scar: Correction of post-infarct arrhythmias through heterotypic cell-cell coupling

doi: 10.1038/s41598-018-25147-8

Figure Lengend Snippet: Lentivirus-mediated Cx43 transduction of SkM results in functional gap junction formation in vitro and in vivo . ( a ) Scheme of the control EGFP and the bicistronic Cx43 lentiviral vectors. ( b ) Immunostainings of cultured, lentivirus transduced EGFP + (green, third panel from left; nuclear Hoechst stain, blue) SkM prove expression of MyoD (white, left panel) and membrane-located Cx43 (red, second panel from left); the right panel is an overlay of all three pictures. ( c ) In vitro dye transfer in differentiated transgenic myotubes (EGFP + , left); patch loading of the upper myotube (arrows) results in progressive dye transfer of Alexa 350 (middle left), but not of Alexa 546-dextran (middle right) into the neighbouring EGFP + SkM (arrowheads). A brightfield image (right) shows a dense monolayer of differentiated and elongated myocytes. ( d , e ) Sirius Red staining of infarcted hearts 12–14 days after the lesion reveals engraftment of EGFP ( d ) and Cx43-EGFP ( e ) ex vivo transduced SkM (fibrotic tissue red, viable cells yellow) in the transmural scar area. Macroscopic imaging and quantitative morphometry revealed in average 19.185 ± 18.743 and 5.338 ± 4.552 engrafted cells in EGFP-SkM and Cx43-SkM engrafted hearts, respectively (n = 5 each). Insets show EGFP + SkM (green, autofluorescence brown) or Cx43 immunostaining (red; nuclear Hoechst stain, blue), of engrafted Cx43-SkM (e, upper right). ( f ) Burst stimulation induces self-terminating VT in a representative EGFP-SkM transplanted mouse in vivo . ( g ) No VT is evoked in a representative Cx43-SkM transplanted mouse upon burst stimulation. ( f , g ) Top trace, surface ECG; bottom trace, atrial intracardiac lead; A, atrium; V, ventricle. ( h ) Statistics of VT incidence upon burst stimulation in vivo reveals prominent reduction of VT inducibility after engraftment of Cx43-SkM compared to EGFP-SkM (p < 0.01). Scale bars: b = 30 µm; c = 200 µm; d,e = 500 µm; d,e insets = 100 µm; e upper right inset = 10 µm.

Article Snippet: As reported before , a surface 6-lead ECG was recorded (PowerLab 16/30, LabChart 7, ADInstruments, Pty LTD, Australia), then the tip of a 2 French octapolar mouse-electrophysiological catheter (CIBER Mouse Electrophysiology Catheter, NuMED, USA) was inserted to the apex of the right ventricle via the right jugular vein.

Techniques: Transduction, Functional Assay, In Vitro, In Vivo, Control, Cell Culture, Staining, Expressing, Membrane, Transgenic Assay, Ex Vivo, Imaging, Immunostaining

Journal: Scientific Reports

Article Title: Overexpression of Cx43 in cells of the myocardial scar: Correction of post-infarct arrhythmias through heterotypic cell-cell coupling

doi: 10.1038/s41598-018-25147-8

Figure Lengend Snippet: Injection of lvCx43 into the myocardial scar strongly lowers post-infarct VT incidence in vivo at 2 weeks after gene therapy ; myocardial remodeling and left ventricular function remain unaltered. ( a – c ) In vivo electrophysiological testing. ( a ) Burst stimulation induces self-limiting VT with typical atrio-ventricular dissociation (lower panel) in a representative lvEGFP injected mouse (upper panel). ( b ) No VT is evoked in a representative lvCx43 transduced mouse upon burst stimulation. (a,b) Top trace, surface ECG; bottom trace, atrial intracardiac lead. ( c ) Magnification of traces shown in (b) reveals appropriate stimulation during the stimulation train, but no VT is induced; due to the short refractory period of murine ventricular myocardium a 3:1 capture during burst stimulation (S1S1 10–50 ms) is achieved. (a–c) A, atrium; V, ventricle. ( d ) In vivo VT incidence after transduction with lvCx43 is significantly reduced compared to lvEGFP injected control hearts (p < 0.02). ( e , f ) lvCx43 and lvEGFP injected hearts display very similar left ventricular function ( e ) and infarct size ( f ).

Article Snippet: As reported before , a surface 6-lead ECG was recorded (PowerLab 16/30, LabChart 7, ADInstruments, Pty LTD, Australia), then the tip of a 2 French octapolar mouse-electrophysiological catheter (CIBER Mouse Electrophysiology Catheter, NuMED, USA) was inserted to the apex of the right ventricle via the right jugular vein.

Techniques: Injection, In Vivo, Transduction, Control

Journal: Scientific Reports

Article Title: Overexpression of Cx43 in cells of the myocardial scar: Correction of post-infarct arrhythmias through heterotypic cell-cell coupling

doi: 10.1038/s41598-018-25147-8

Figure Lengend Snippet: Injection of lvCx43 into the myocardial scar increases conduction in Langendorff-perfused hearts and provides long time protection against VT in vivo . ( a – d ) Optical mapping ( a ) Overview of a representative lvEGFP injected heart (leftmost panel, infarct region is encircled). Under sinus rhythm and unipolar pacing from the base of the heart, sequential di-4-ANNEPS fluorescence images display highly irregular and atypical conduction paths surrounding the lesioned area (images every 11 ms). ( b ) Also lvCx43 injected hearts revealed atypical propagation patterns, but some conduction through the scar area is visible (images every 8 ms). ( c ) Isochronal maps (same hearts as in a and b) depicting the activation wavefront and conduction delays near the infarct border zone. The activation bypasses the lvEGFP injected infarct (upper panel), but propagates through the lesioned area in the lvCx43 injected heart (lower panel); H, healthy; B, border zone; I, infarct. Scale bar indicates local activation times. ( d ) Local conduction velocities at 200 ms pacing. Note its significant increase in the infarct area (p = 0.0173) of lvCx43 injected hearts (n = 5) vs lvEGFP injected control hearts (n = 5). ( e , f ) Representative traces during in vivo burst stimulation 2 months after lentiviral gene transfer recorded from a lvEGFP ( e ) and a lvCx43 ( f ) injected heart. In the lvEGFP heart onset of VT shortly upon burst stimulation is observed (e), whereas no VT is induced in the lvCx43 heart (f); Top trace, surface ECG; bottom trace, atrial intracardiac lead; A, atrium; V, ventricle. ( g ) Statistical analysis of VT incidence shows a significantly (p < 0.05) lower incidence in the lvCx43 compared to lvEGFP control hearts. ( h , i ) There is no difference in left ventricular function (fractional shortening, h ) and infarct size ( i ) between lvEGFP and lvCx43 injected hearts 8 weeks after gene therapy.

Article Snippet: As reported before , a surface 6-lead ECG was recorded (PowerLab 16/30, LabChart 7, ADInstruments, Pty LTD, Australia), then the tip of a 2 French octapolar mouse-electrophysiological catheter (CIBER Mouse Electrophysiology Catheter, NuMED, USA) was inserted to the apex of the right ventricle via the right jugular vein.

Techniques: Injection, In Vivo, Fluorescence, Activation Assay, Control