Effects of diacetyl monoxime and cytochalasin D on ventricular fibrillation in swine right ventricles

2001 ◽  
Vol 280 (6) ◽  
pp. H2689-H2696 ◽  
Author(s):  
Moon-Hyoung Lee ◽  
Shien-Fong Lin ◽  
Toshihiko Ohara ◽  
Chikaya Omichi ◽  
Yuji Okuyama ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Ventricular Fibrillation ◽  
Action Potential Duration ◽  
Action Potentials ◽  
Optical Mapping ◽  
Cytochalasin D ◽  
Wave Fronts ◽  
Activation Patterns ◽  
Restitution Curve ◽  
Diacetyl Monoxime

Whether or not the excitation-contraction (E-C) uncoupler diacetyl monoxime (DAM) and cytochalacin D (Cyto D) alter the ventricular fibrillation (VF) activation patterns is unclear. We recorded single cell action potentials and performed optical mapping in isolated perfused swine right ventricles (RV) at different concentrations of DAM and Cyto D. Increasing the concentration of DAM results in progressively shortened action potential duration (APD) measured to 90% repolarization, reduced the slope of the APD restitition curve, decreased Kolmogorov-Sinai entropy, and reduced the number of VF wave fronts. In all RVs, 15–20 mmol/l DAM converted VF to ventricular tachycardia (VT). The VF could be reinduced after the DAM was washed out. In comparison, Cyto D (10–40 μmol/l) has no effects on APD restitution curve or the dynamics of VF. The effects of DAM on VF are associated with a reduced number of wave fronts and dynamic complexities in VF. These results are compatible with the restitution hypothesis of VF and suggest that DAM may be unsuitable as an E-C uncoupler for optical mapping studies of VF in the swine RVs.

Effects of amiodarone on wave front dynamics during ventricular fibrillation in isolated swine right ventricle

2002 ◽  
Vol 282 (3) ◽  
pp. H1063-H1070 ◽  
Author(s):  
Chikaya Omichi ◽  
Shengmei Zhou ◽  
Moon-Hyoung Lee ◽  
Ajay Naik ◽  
Che-Ming Chang ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Wave Front ◽  
Action Potentials ◽  
Cycle Length ◽  
Core Size ◽  
Wave Fronts ◽  
Activation Patterns ◽  
In Vitro Activation ◽  
Front Dynamics

The effects of acute amiodarone infusion on dynamics of ventricular fibrillation (VF) are unclear. Six isolated swine right ventricles (RVs) were studied in vitro. Activation patterns during VF were mapped optically, whereas action potentials were recorded with a glass microelectrode. At baseline, VF was associated with frequent spontaneous wave breaks. Amiodarone (2.5 μg/ml) reduced spontaneous wave breaks and increased the cycle length (CL) of VF from 83.3 ± 17.8 ms at baseline to 118.4 ± 25.8 ms during infusion ( P < 0.05). Amiodarone increased the reentrant wave front CL (114.4 ± 15.5 vs. 78.2 ± 19.0 ms, P < 0.05) and central core area (4.1 ± 3.8 vs. 0.9 ± 0.3 mm2, P < 0.05). Within 30 min of infusion, VF terminated ( n = 1), converted to ventricular tachycardia (VT) ( n = 1) or continued at a slower rate ( n = 4). Amiodarone flattened the APD restitution curves. We conclude that amiodarone reduced spontaneous wave breaks. It might terminate VF or convert VF to VT. These effects were associated with the flattening of APD restitution slope and increased core size of reentrant wave fronts.

Optical mapping of late myocardial infarction in rats

2006 ◽  
Vol 290 (3) ◽  
pp. H1298-H1306 ◽  
Author(s):  
William R. Mills ◽  
Niladri Mal ◽  
Farhad Forudi ◽  
Zoran B. Popovic ◽  
Marc S. Penn ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Tachycardia ◽  
High Resolution ◽  
Action Potentials ◽  
Optical Mapping ◽  
Cellular Heterogeneity ◽  
Artery Ligation ◽  
Conduction Abnormalities ◽  
Mapping Techniques ◽  
Whole Heart

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.

Effects of heart isolation, voltage-sensitive dye, and electromechanical uncoupling agents on ventricular fibrillation

2003 ◽  
Vol 284 (5) ◽  
pp. H1818-H1826 ◽  
Author(s):  
Hao Qin ◽  
Matthew W. Kay ◽  
Nipon Chattipakorn ◽  
David T. Redden ◽  
Raymond E. Ideker ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Pattern Analysis ◽  
Electrode Array ◽  
Left Ventricular ◽  
Control Data ◽  
Voltage Sensitive Dye ◽  
Activation Patterns ◽  
Langendorff Perfusion ◽  
Perfusion Apparatus ◽  
Diacetyl Monoxime

We tested whether the interventions typically required for optical mapping affect activation patterns during ventricular fibrillation (VF). A 21 × 24 unipolar electrode array (1.5 mm spacing) was sutured to the left ventricular epicardium of 16 anesthetized pigs, and four episodes of electrically induced VF (30-s duration) were recorded. The hearts were then rapidly excised and connected to a Langendorff perfusion apparatus. Four of the hearts were controls, in which 24 additional VF episodes were then mapped. In the remaining 12 hearts, four VF episodes were mapped after isolation, four more episodes were mapped after exposure to the voltage-sensitive dye di-4-ANEPPS, and six more episodes were mapped after exposure to the electromechanical uncoupling agents diacetyl monoxime (DAM; 20 mmol/l, n = 6) or cytochalasin D (CytoD; 10 μmol/l, n = 6). VF episodes were separated by 4 min. VF activation patterns were quantified using custom pattern analysis algorithms. From comparisons with time-corrected control data, all interventions significantly changed VF patterns. Most changes were broadly consistent with slowing and regularization due to loss of excitability. Heart isolation had the largest effect on VF patterns, followed by CytoD, DAM, and dye.

Effects of mechanical uncouplers, diacetyl monoxime, and cytochalasin-D on the electrophysiology of perfused mouse hearts

2004 ◽  
Vol 287 (4) ◽  
pp. H1771-H1779 ◽  
Author(s):  
Linda C. Baker ◽  
Robert Wolk ◽  
Bum-Rak Choi ◽  
Simon Watkins ◽  
Patricia Plan ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Cytochalasin D ◽  
Emission Wavelength ◽  
Excitation Wavelength ◽  
Dependent Manner ◽  
Refractory Periods ◽  
Intracellular Ca ◽  
Diacetyl Monoxime ◽  
Confocal Images ◽  
20 Nm

Chemical uncouplers diacetyl monoxime (DAM) and cytochalasin D (cyto-D) are used to abolish cardiac contractions in optical studies, yet alter intracellular Ca2+ concentration ([Ca2+]i) handling and vulnerability to arrhythmias in a species-dependent manner. The effects of uncouplers were investigated in perfused mouse hearts labeled with rhod-2/AM or 4-[β-[2-(di- n-butylamino)-6-naphthyl]vinyl]pyridinium (di-4-ANEPPS) to map [Ca2+]i transients (emission wavelength = 585 ± 20 nm) and action potentials (APs) (emission wavelength > 610 nm; excitation wavelength = 530 ± 20 nm). Confocal images showed that rhod-2 is primarily in the cytosol. DAM (15 mM) and cyto-D (5 μM) increased AP durations (APD75 = 20.0 ± 3 to 46.6 ± 5 ms and 39.9 ± 8 ms, respectively, n = 4) and refractory periods (45.14 ± 12.1 to 82.5 ± 3.5 ms and 78 ± 4.24 ms, respectively). Cyto-D reduced conduction velocity by 20% within 5 min and DAM by 10% gradually in 1 h ( n = 5 each). Uncouplers did not alter the direction and gradient of repolarization, which progressed from apex to base in 15 ± 3 ms. Peak systolic [Ca2+]i increased with cyto-D from 743 ± 47 ( n = 8) to 944 ± 17 nM ( n = 3, P = 0.01) but decreased with DAM to 398 ± 44 nM ( n = 3, P < 0.01). Diastolic [Ca2+]i was higher with cyto-D (544 ± 80 nM, n = 3) and lower with DAM (224 ± 31, n = 3) compared with controls (257 ± 30 nM, n = 3). DAM prolonged [Ca2+]i transients at 75% recovery (54.3 ± 5 to 83.6 ± 1.9 ms), whereas cyto-D had no effect (58.6 ± 1.2 ms; n = 3). Burst pacing routinely elicited long-lasting ventricular tachycardia but not fibrillation. Uncouplers flattened the slope of AP restitution kinetic curves and blocked ventricular tachycardia induced by burst pacing.

Optical mapping of Langendorff-perfused human hearts: establishing a model for the study of ventricular fibrillation in humans

2007 ◽  
Vol 293 (1) ◽  
pp. H875-H880 ◽  
Author(s):  
Kumaraswamy Nanthakumar ◽  
José Jalife ◽  
Stéphane Massé ◽  
Eugene Downar ◽  
Mihaela Pop ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Optical Mapping ◽  
Signal To Noise Ratio ◽  
Wave Fronts ◽  
Mean Velocity ◽  
Optical Signals ◽  
Emission Signal ◽  
Halogen Light ◽  
Halogen Light Source ◽  
Singularity Point

Our objective was to establish a novel model for the study of ventricular fibrillation (VF) in humans. We adopted the established techniques of optical mapping to human ventricles for the first time to determine whether human VF is the result of wave breaks and singularity point formation and is maintained by high-frequency rotors and fibrillatory conduction. We describe the technique of acquiring optical signals in human hearts during VF, their characteristics, and the feasibility of possible analyses that could be performed to elucidate mechanisms of human VF. We used explanted hearts from five cardiomyopathic patients who underwent transplantation. The hearts were Langendorff perfused with Tyrode solution (95% O2-5% CO2), and the potentiometric dye di-4-ANEPPS was injected as a bolus into the coronary circulation. Fluorescence was excited at 531 ± 20 nm with a 150-W halogen light source; the emission signal was long-pass filtered at 610 nm and recorded with a mapping camera. Fractional change of fluorescence varied between 2% and 12%. Average signal-to-noise ratio was 40 dB. The mean velocity of VF wave fronts was 0.25 ± 0.04 m/s. Submillimetric spatial resolution (0.65–0.85 mm), activation mapping, and transformation of the data to phase-based analysis revealed reentrant, colliding, and fractionating wave fronts in human VF. On many occasions the VF wave fronts were as large as the entire vertical length (8 cm) of the mapping field, suggesting that there are a limited number of wave fronts on the human heart during VF. Phase transformation of the optical signals allowed the first demonstration ever of phase singularity point, wave breaks, and rotor formation in human VF. This method provides opportunities for potential analyses toward elucidation of the mechanisms of VF and defibrillation in humans.

Action potential duration restitution and ventricular fibrillation due to rapid focal excitation

2002 ◽  
Vol 282 (5) ◽  
pp. H1915-H1923 ◽  
Author(s):  
Moshe Swissa ◽  
Zhilin Qu ◽  
Toshihiko Ohara ◽  
Moon-Hyoung Lee ◽  
Shien-Fong Lin ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Action Potential ◽  
Action Potential Duration ◽  
Cardiac Tissue ◽  
Diacetyl Monoxime ◽  
Focal Excitation ◽  
Mean Cycle ◽  
Rapid Activation ◽  
Action Potential Duration Restitution ◽  
Wave Break

The focal source hypothesis of ventricular fibrillation (VF) posits that rapid activation from a focal source, rather than action potential duration (APD) restitution properties, is responsible for the maintenance of VF. We injected aconitine (100 μg) into normal isolated perfused swine right ventricles (RVs) stained with 4-{β-[2-(di- n-butylamino)-6-naphthyl]vinyl}pyridinium (di-4-ANEPPS) for optical mapping studies. Within 97 ± 163 s, aconitine induced ventricular tachycardia (VT) with a mean cycle length 268 ± 37 ms, which accelerated before converting to VF. Drugs that flatten the APD restitution slope, including diacetyl monoxime (10–20 mM, n = 6), bretylium (10–20 μg/ml, n = 3), and verapamil (2–4 μg/ml, n = 3), reversibly converted VF to VT in all cases. In two RVs, VF persisted despite of the excision of the aconitine site. Simulations in two-dimensional cardiac tissue showed that once VF was initiated, it remained sustained even after the “aconitine” site was eliminated. In this model of focal source VF, the VT-to-VF transition occurred due to a wave break outside the aconitine site, and drugs that flattened the APD restitution slope converted VF to VT despite continuous activation from aconitine site.

Pulseless ventricular tachycardia and ventricular fibrillation complicating severe traumatic brain injury in pediatrics

2019 ◽  
Vol 85 (12) ◽  
Author(s):  
Marco Piastra ◽  
Luca Tortorolo ◽  
Orazio Genovese ◽  
Tony C. Morena ◽  
Enzo Picconi ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Ventricular Tachycardia ◽  
Brain Injury ◽  
Ventricular Fibrillation ◽  
Severe Traumatic Brain Injury
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