Monophasic action potential recordings in response to graded hyperkalemia in dogs

1989 ◽  
Vol 256 (4) ◽  
pp. H956-H961
Author(s):  
P. M. Sutton ◽  
P. Taggart ◽  
D. W. Spear ◽  
H. F. Drake ◽  
R. H. Swanton ◽  
...  
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Regional Differences ◽  
Monophasic Action Potential ◽  
Extracellular Potassium ◽  
Activation Time ◽  
Biphasic Response ◽  
The Difference ◽  
Alpha Chloralose

Recent interest in sudden cardiac death during exercise in normal healthy people has highlighted the possible role of swings of extracellular potassium in arrhythmogenesis in conditions other than ischemia. Regional differences in action potential duration and conduction may be important. We have recorded monophasic action potentials (MAPs) from the endocardium and epicardium in nine open-chest dogs during graded intravenous infusion of potassium up to a plasma level of 9 mM. The animals were anesthetized with alpha-chloralose and urethan. Continuous, online arterial potassium monitoring was employed. MAP duration showed a biphasic response with initial shortening up to 7 mM, which tended to be more obvious on the epicardium. Regional activation time was measured as the difference between the onset of depolarization of the endocardial and epicardial MAP. Regional activation time also showed a biphasic response with initial shortening and subsequent delay. The QRS width of the scalar lead II electrocardiogram also showed biphasic changes, and the T wave amplitude progressively decreased. Our results suggest that regional differences in repolarization time may develop in the nonischemic myocardium in response to increased extracellular potassium levels mainly as a result of local changes in regional activation time rather than as a result of a direct effect on action potential duration.

Effects of Thoracic Epidural Anesthesia with and without Autonomic Nervous System Blockade on Cardiac Monophasic Action Potentials and Effective Refractoriness in Awake Dogs

2001 ◽  
Vol 95 (1) ◽  
pp. 132-138 ◽  
Author(s):  
Andreas Meissner ◽  
Lars Eckardt ◽  
Paulus Kirchhof ◽  
Thomas Weber ◽  
Norbert Rolf ◽  
...  
Keyword(s):  
Action Potential ◽  
Epidural Anesthesia ◽  
Action Potential Duration ◽  
Action Potentials ◽  
Monophasic Action Potential ◽  
Thoracic Epidural Anesthesia ◽  
Thoracic Epidural ◽  
Monophasic Action Potentials ◽  
Cycle Lengths

Background The effects of thoracic epidural anesthesia (TEA) on myocardial repolarization and arrhythmogenicity are only incompletely understood. This is primarily because of the lack of appropriate experimental models. In most of the studies performed thus far, TEA was used in anesthetized animals. Baseline anesthesia itself may have modified the effects of TEA. This study investigates right atrial and ventricular repolarization by recording monophasic action potentials after TEA in awake dogs. The authors hypothesized that an antiarrhythmic role of TEA exists, which may be related to a direct effect of TEA on myocardial repolarization. Methods The hypothesis was tested in an in vivo canine model, in which atrial and ventricular myocardial action potential duration and refractoriness are recorded by means of monophasic action potential catheters. Results Thoracic epidural anesthesia significantly increased ventricular monophasic action potential duration for cycle lengths shorter than 350 ms. Changes in monophasic action potential duration were paralleled by a concomitant prolongation of effective refractory period (ERP) at higher rates so that the ratio of ERP to action potential duration was unaffected. Conclusions This model helps to study the role of TEA on ventricular repolarization and arrhythmogenicity. Because lengthening of repolarization and prolongation of refractoriness may, in some circumstances, be antiarrhythmic, TEA may be protective against generation of ventricular arrhythmias mediated, e.g., by increased sympathetic tone. The results also imply that the beneficial role of TEA might be stronger at the ventricular site as compared with the atrium. At atrial sites there was only a trend toward prolongation of repolarization even at short cycle lengths.

Effect of sotalol, aprindine and the combination aprindine—sotalol on monophasic action potential duration

1986 ◽  
Vol 7 (1) ◽  
pp. 47-53 ◽  
Author(s):  
R. STROOBANDT ◽  
J. BRACHMANN ◽  
H. KESTELOOT ◽  
W. KÜBLER ◽  
J. SENGES
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Monophasic Action Potential

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.

Acetylcholine release by a stimulus train lowers atrial fibrillation threshold

1987 ◽  
Vol 253 (4) ◽  
pp. H863-H868 ◽  
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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