Reflex vagal control of atrial repolarization

The reflex vagal control of atrial repolarization was investigated in eight open-chest, anesthetized dogs. A monophasic action potential was recorded from the right atrium, and the action potential duration to 90% repolarization (APD90) was determined every cardiac cycle. beta-Adrenergic receptors were blocked with timolol (0.1 mg/kg). Under baseline conditions, sinus slowing during sinus arrhythmia was accompanied by a significant shortening of APD90 (24 +/- 4.0 ms). Transient occlusion (30 s) of the descending thoracic aorta increased systolic aortic pressure from 138 +/- 2.8 to 181 +/- 3.3 mmHg (P < 0.01). Heart rate decreased from 99 +/- 3.6 to 42.5 +/- 3.4 beats/min (P < 0.01), and APD90 shortened from 168 +/- 5.1 to 94 +/- 3.3 ms (P < 0.01). Release of the occlusion caused arterial hypotension (95 +/- 2.8 mmHg) and an overshoot in both rate (126 +/- 5.2 beats/min) and APD90 (189 +/- 2.3 ms). Aortic occlusion during atrial pacing (130-160 beats/min) decreased APD90 from 147 +/- 7.0 to 78 +/- 3.4 ms (P < 0.01). Cervical vagotomy or atropine eliminated changes in rate and APD90 evoked by aortic occlusion. The results indicate that there is parallel central vagal control of both sinus rate and atrial repolarization. Sinus bradycardia during reflex vagal activation does not prevent the acceleration of atrial repolarization.

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Dispersion of monophasic action potential durations and activation times during atrial pacing, ventricular pacing, and ventricular premature stimulation in canine ventricles

Cardiovascular Research ◽

10.1093/cvr/17.3.152 ◽

1983 ◽

Vol 17 (3) ◽

pp. 152-161 ◽

Cited By ~ 59

Author(s):

C.-S. KUO ◽

J. P. AMLIE ◽

K. MUNAKATA ◽

C P. REDDY ◽

B. SURAWICZ

Keyword(s):

Action Potential ◽

Monophasic Action Potential ◽

Atrial Pacing ◽

Ventricular Pacing ◽

Activation Times

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Regional electromechanical alternans in anesthetized pig hearts: modulation by mechanoelectric feedback

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.267.5.h1726 ◽

1994 ◽

Vol 267 (5) ◽

pp. H1726-H1735 ◽

Cited By ~ 1

Author(s):

C. F. Murphy ◽

M. J. Lab ◽

S. M. Horner ◽

D. J. Dick ◽

F. G. Harrison

Keyword(s):

Left Ventricle ◽

Action Potential ◽

Monophasic Action Potential ◽

Mechanical Activity ◽

Strain Gauges ◽

Atrial Pacing ◽

Mechanoelectric Feedback ◽

Pulsus Alternans ◽

Electrical Alternans ◽

Intact Heart

Electrical and mechanical alternans have often been found to coexist. However, the factors controlling their interdependence are not known. In this study we measure regional electrical and mechanical activity during mechanical alternans to investigate this relationship. Mechanical alternans was induced by rapid atrial pacing in 18 anesthetized, open-chest pigs. Regional segmental contraction and monophasic action potential were measured in three areas of left ventricle using epicardial tripodal strain gauges and suction electrodes. Electrical alternans always accompanied pulsus alternans. The phase of electrical alternans was not related to any measure of regional mechanical activity but did show a constant discordant relation to peak ventricular pressure. This suggested that mechanically dependent changes in action potential duration (mechanoelectric feedback) may be important in modulation electrical alternans. In support of this, pulsus alternans simulated by clamping the proximal aorta on alternate beats was associated with electrical alternans comparable to that produced with rapid atrial pacing. Mechanoelectric feedback modulates regional electrophysiology in the intact heart and may be important in the generation of electrical alternans.

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Acetylcholine release by a stimulus train lowers atrial fibrillation threshold

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1987.253.4.h863 ◽

1987 ◽

Vol 253 (4) ◽

pp. H863-H868 ◽

Cited By ~ 2

Author(s):

D. E. Euler ◽

P. J. Scanlon

Keyword(s):

Atrial Fibrillation ◽

Action Potential ◽

Right Atrium ◽

Single Pulse ◽

Monophasic Action Potential ◽

Adrenergic Blockade ◽

The Right ◽

Alpha Chloralose ◽

Electrical Stimuli ◽

Local Release

This study was designed to evaluate the importance of local release of autonomic neuromediators when electrical stimuli are applied to the right atrium to measure the atrial fibrillation threshold (AFT). Experiments were performed in 16 open-chest dogs anesthetized with alpha-chloralose. The dogs were denervated by bilateral transection of the stellates and cervical vagi. The AFT was determined in 11 dogs by delivering either a train of stimuli (14 pulses, 4 ms, 100 Hz) or a single stimulus (10 ms) to the right atrium during its vulnerable period. In eight dogs, beta-adrenergic blockade with timolol (0.1 mg/kg) had no effect on the AFT determined with either method. Atropine (0.2 mg/kg), given after timolol, significantly increased the train-of-pulses AFT from 4.7 +/- 0.4 to 32.3 +/- 4.6 mA (P less than 0.001). The single-pulse AFT increased from 16.5 +/- 1.5 to 17.8 +/- 1.5 mA (P less than 0.05). Atropine had a similar effect on the AFT when it was given in the absence of timolol (n = 3). In five additional dogs, a monophasic action potential was recorded while a 10-mA train was delivered to the atrium during its absolute refractory period. There was marked shortening of the monophasic action potential duration (55 +/- 6 ms) in the first beat after the train. The shortening was totally abolished by atropine (0.2 mg/kg). The results suggest that a train of stimuli liberates local stores of acetylcholine, which cause a shortening of atrial repolarization time and a profound decrease in the current necessary to evoke fibrillation.

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The thyroid hormone analog DITPA restoresI to in rats after myocardial infarction

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2000.278.4.h1105 ◽

2000 ◽

Vol 278 (4) ◽

pp. H1105-H1116 ◽

Cited By ~ 21

Author(s):

Alan D. Wickenden ◽

Roger Kaprielian ◽

Xiao-Mang You ◽

Peter H. Backx

Keyword(s):

Myocardial Infarction ◽

Thyroid Hormone ◽

Action Potential ◽

Ventricular Myocytes ◽

Monophasic Action Potential ◽

Mrna Levels ◽

Hormone Analog ◽

Life Threatening ◽

The Right

Previous studies have established that reductions in repolarizing currents occur in heart disease and can contribute to life-threatening arrhythmias in myocardium. In this study, we investigated whether the thyroid hormone analog 3,5-diiodothyropropionic acid (DITPA) could restore repolarizing transient outward K+ current ( I to) density and gene expression in rat myocardium after myocardial infarction (MI). Our findings show that I to density was reduced after MI (14.0 ± 1.0 vs. 10.2 ± 0.9 pA/pF, sham vs. post-MI at +40 mV). mRNA levels of Kv4.2 and Kv4.3genes were decreased but Kv1.4 mRNA levels were increased post-MI. Corresponding changes in Kv4.2 and Kv1.4 protein were also observed. Chronic treatment of post-MI rats with 10 mg/kg DITPA restored I to density (to 15.2 ± 1.1 pA/pF at +40 mV) as well as Kv4.2 and Kv1.4 expression to levels observed in sham-operated controls. Other membrane currents (Na+, L-type Ca2+, sustained, and inward rectifier K+ currents) were unaffected by DITPA treatment. Associated with the changes in I toexpression, action potential durations (current-clamp recordings in isolated single right ventricular myocytes and monophasic action potential recordings from the right free wall in situ) were prolonged after MI and restored with DITPA treatment. Our results demonstrate that DITPA restores I to density in the setting of MI, which may be useful in preventing complications associated with I to downregulation.

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Quinidine elicits proarrhythmic changes in ventricular repolarization and refractoriness in guinea-pig

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2012-0379 ◽

2013 ◽

Vol 91 (4) ◽

pp. 306-315 ◽

Cited By ~ 15

Author(s):

Oleg E. Osadchii

Keyword(s):

Guinea Pig ◽

Action Potential ◽

Left Ventricular ◽

Ventricular Repolarization ◽

Monophasic Action Potential ◽

Delayed Rectifier ◽

Rate Dependent ◽

Delayed Rectifier Current ◽

Left Ventricular Chamber ◽

The Right

Quinidine is a class Ia Na+ channel blocker that prolongs cardiac repolarization owing to the inhibition of IKr, the rapid component of the delayed rectifier current. Although quinidine may induce proarrhythmia, the contributing mechanisms remain incompletely understood. This study examined whether quinidine may set proarrhythmic substrate by inducing spatiotemporal abnormalities in repolarization and refractoriness. The monophasic action potential duration (APD), effective refractory periods (ERPs), and volume-conducted electrocardiograms (ECGs) were assessed in perfused guinea-pig hearts. Quinidine was found to produce the reverse rate-dependent prolongation of ventricular repolarization, which contributed to increased steepness of APD restitution. Throughout the epicardium, quinidine elicited a greater APD increase in the left ventricular chamber compared with the right ventricle, thereby enhancing spatial repolarization heterogeneities. Quinidine prolonged APD to a greater extent than ERP, thus extending the vulnerable window for ventricular re-excitation. This change was attributed to increased triangulation of epicardial action potential because of greater APD lengthening at 90% repolarization than at 30% repolarization. Over the transmural plane, quinidine evoked a greater ERP prolongation at endocardium than epicardium and increased dispersion of refractoriness. Premature ectopic beats and monomorphic ventricular tachycardia were observed in 50% of quinidine-treated heart preparations. In summary, abnormal changes in repolarization and refractoriness contribute greatly to proarrhythmic substrate upon quinidine infusion.

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