scholarly journals Cardiac contractility modulation increases action potential duration dispersion and decreases ventricular fibrillation threshold via β1-adrenoceptor activation in the crystalloid perfused normal rabbit heart

2014 ◽  
Vol 172 (1) ◽  
pp. 144-154 ◽  
Author(s):  
James Winter ◽  
Kieran E. Brack ◽  
John H. Coote ◽  
G. André Ng
Keyword(s):  
Ventricular Fibrillation ◽  
Action Potential ◽  
Action Potential Duration ◽  
Cardiac Contractility ◽  
Rabbit Heart ◽  
Cardiac Contractility Modulation ◽  
Ventricular Fibrillation Threshold

scholarly journals 706-4 Preconditioning Shortens Action Potential Duration and Lowers Ventricular Fibrillation Threshold in Pig Hearts

1995 ◽  
Vol 25 (2) ◽  
pp. 43A
Author(s):  
Michel Ovize ◽  
Jean F Aupetit ◽  
Gilles Rioufol ◽  
Joseph Loufoua ◽  
Xavier André-Fouët ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Action Potential ◽  
Action Potential Duration ◽  
Ventricular Fibrillation Threshold

Preconditioning reduces infarct size but accelerates time to ventricular fibrillation in ischemic pig heart

1995 ◽  
Vol 269 (1) ◽  
pp. H72-H79 ◽  
Author(s):  
M. Ovize ◽  
J. F. Aupetit ◽  
G. Rioufol ◽  
J. Loufoua ◽  
X. Andre-Fouet ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Action Potential ◽  
Infarct Size ◽  
Action Potential Duration ◽  
Ventricular Arrhythmias ◽  
Monophasic Action Potential ◽  
Control Group ◽  
Large Animal ◽  
Large Animal Models ◽  
Ventricular Fibrillation Threshold

Preconditioning protects the rat heart from ventricular arrhythmias. However, the mechanism of this beneficial effect and its existence in large animal models remain unknown. We submitted 49 pigs to 40 min of left anterior descending coronary occlusion and 2 h of reperfusion and assessed the incidence of ventricular fibrillation (VF) and time to VF. Monophasic action potential duration (MAPD) and ventricular fibrillation threshold (VFT) were measured throughout the experiment. Preconditioning significantly reduced infarct size but failed to reduce the incidence of VF either during the 40-min ischemic insult or the following reperfusion. Moreover, preconditioning accelerated the onset of VF during the prolonged ischemia; time to VF averaged 8 +/- 2 min in the preconditioned group vs. 18 +/- 2 min in the control group (P < 0.05). This premature peak of VF in preconditioned hearts was associated with a significant decrease of VFT and shortening of MAPD. This suggests that preconditioning does not limit the incidence of VF in the pig model. Rather, preconditioning decreases the time to VF in this species, likely through lowering of the VFT and shortening of the action potential duration.

scholarly journals Intramural optical mapping of Vm and Cai2+ during long-duration ventricular fibrillation in canine hearts

2012 ◽  
Vol 302 (6) ◽  
pp. H1294-H1305 ◽  
Author(s):  
Wei Kong ◽  
Raymond E. Ideker ◽  
Vladimir G. Fast
Keyword(s):  
Ventricular Fibrillation ◽  
Action Potential ◽  
Short Duration ◽  
Action Potential Duration ◽  
Cycle Length ◽  
The Other ◽  
Membrane Voltage ◽  
Long Duration ◽  
Intracellular Ca ◽  
Rapid Pacing

Intramural gradients of intracellular Ca2+ (Cai2+) Cai2+ handling, Cai2+ oscillations, and Cai2+ transient (CaT) alternans may be important in long-duration ventricular fibrillation (LDVF). However, previous studies of Cai2+ handling have been limited to recordings from the heart surface during short-duration ventricular fibrillation. To examine whether abnormalities of intramural Cai2+ handling contribute to LDVF, we measured membrane voltage ( Vm) and Cai2+ during pacing and LDVF in six perfused canine hearts using five eight-fiber optrodes. Measurements were grouped into epicardial, midwall, and endocardial layers. We found that during pacing at 350-ms cycle length, CaT duration was slightly longer (by ≃10%) in endocardial layers than in epicardial layers, whereas action potential duration (APD) exhibited no difference. Rapid pacing at 150-ms cycle length caused alternans in both APD (APD-ALT) and CaT amplitude (CaA-ALT) without significant transmural differences. For 93% of optrode recordings, CaA-ALT was transmurally concordant, whereas APD-ALT was either concordant (36%) or discordant (54%), suggesting that APD-ALT was not caused by CaA-ALT. During LDVF, Vm and Cai2+ progressively desynchronized when not every action potential was followed by a CaT. Such desynchronization developed faster in the epicardium than in the other layers. In addition, CaT duration strongly increased (by ∼240% at 5 min of LDVF), whereas APD shortened (by ∼17%). CaT rises always followed Vm upstrokes during pacing and LDVF. In conclusion, the fact that Vm upstrokes always preceded CaTs indicates that spontaneous Cai2+ oscillations in the working myocardium were not likely the reason for LDVF maintenance. Strong Vm-Cai2+ desynchronization and the occurrence of long CaTs during LDVF indicate severely impaired Cai2+ handling and may potentially contribute to LDVF maintenance.

scholarly journals Idiopathic Ventricular Fibrillation Characterized by Spatial Heterogeneity of Action Potential Duration and Its Restitution Kinetics

2008 ◽  
Vol 49 (6) ◽  
pp. 733-740 ◽  
Author(s):  
Sonoko Ashino ◽  
Ichiro Watanabe ◽  
Masayoshi Kofune ◽  
Kimie Ohkubo ◽  
Yasuo Okumura ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Action Potential ◽  
Spatial Heterogeneity ◽  
Action Potential Duration ◽  
Idiopathic Ventricular Fibrillation

Mechanism of atrioventricular nodal facilitation in the rabbit heart: role of the distal AV node

1997 ◽  
Vol 272 (6) ◽  
pp. H2815-H2825 ◽  
Author(s):  
G. J. Fahy ◽  
I. Efimov ◽  
Y. Cheng ◽  
G. A. Kidwell ◽  
D. Van Wagoner ◽  
...  
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Cellular Response ◽  
Rabbit Heart ◽  
Av Node ◽  
Microelectrode Recordings ◽  
Bundle Of His ◽  
Action Potential Shortening

We investigated whether atrioventricular (AV) nodal facilitation is the result of distal AV nodal action potential shortening. Atrial and bundle of His (H) electrograms and microelectrode recordings from proximal and distal AV nodal cells were analyzed in eight superfused rabbit AV node preparations in response to two pacing protocols. In the facilitation protocol, an atrial extrastimulus (A3) was preceded by an atrial impulse (A2) introduced 300, 200, 150, or 125 ms after 30 basic beats (A1). The preexcitation protocol differed from the facilitation protocol by the addition of a premature His depolarization (h2) such that the H1-h2 interval was shorter than the H1-H2 interval. Conduction curves (A3-H3 vs. H2-A3, h2-A3, and A2-A3 intervals) were constructed. Facilitation was demonstrated in all preparations when H2-A3 was used (P = 0.02) but not in the A2-A3 format. Compared with facilitation at the same A1-A2 intervals, preexcitation, despite shortening the distal cellular action potential duration, resulted in longer A3-H3 delays (P = 0.002), shorter A2-A3 intervals, and depression of the proximal nodal cellular response. Thus facilitation does not result from altered distal AV nodal characteristics and instead is a manifestation of an uncontrolled pacing protocol-dependent modulation of proximal AV nodal function.

Effects of [K+]o on electrical restitution and activation dynamics during ventricular fibrillation

2000 ◽  
Vol 279 (6) ◽  
pp. H2665-H2672 ◽  
Author(s):  
Marcus L. Koller ◽  
Mark L. Riccio ◽  
Robert F. Gilmour
Keyword(s):  
Ventricular Fibrillation ◽  
Action Potential ◽  
Action Potential Duration ◽  
Maximum Amplitude ◽  
Spatiotemporal Organization ◽  
Activation Dynamics ◽  
Spontaneous Frequency ◽  
Upstroke Velocity

To test whether hyperkalemia suppresses ventricular fibrillation (VF) by reducing the slope of the action potential duration (APD) restitution relation, we determined the effects of the extracellular K+concentration ([K+]o) ([KCl] = 2.7–12 mM) on the restitution of APD and maximum upstroke velocity ( V max) the magnitude of APD alternans and spatiotemporal organization during VF in isolated canine ventricle. As [KCl] was increased incrementally from 2.7 to 12 mM, V max was reduced progressively. Increasing [KCl] from 2.7 to 10 mM decreased the slope of the APD restitution relation at long, but not short, diastolic intervals (DI), decreased the range of DI over which the slope was ≥1, and reduced the maximum amplitude of APD alternans. At [KCl] = 12 mM, the range of DI over which the APD restitution slope was ≥1 increased, and the maximum amplitude of APD alternans increased. For [KCl] = 4–8 mM, the persistence of APD alternans at short DI was associated with maintenance of VF. For [KCl] = 10–12 mM, the spontaneous frequency during VF was reduced, and activation occurred predominantly at longer DI. The lack of APD alternans at longer DI was associated with conversion of VF to a periodic rhythm. These results provide additional evidence for the importance of APD restitution kinetics in the development of VF.

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