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.

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

1997 ◽  
Vol 273 (4) ◽  
pp. H1658-H1668 ◽  
Author(s):  
Todor Mazgalev ◽  
Kent Mowrey ◽  
Igor Efimov ◽  
Gerard J. Fahy ◽  
David Van Wagoner ◽  
...  
Keyword(s):  
Cellular Response ◽  
Cycle Length ◽  
Cellular Responses ◽  
Rabbit Heart ◽  
Black Box ◽  
Av Node ◽  
Functional Studies ◽  
Microelectrode Recordings ◽  
Coupling Interval

The phenomenon of atrioventricular (AV) nodal “facilitation,” described in traditional “black box”-functional studies, implies enhanced AV nodal dromotropic function. We investigated the role of atrial prematurities in the modulation of the nodal cellular responses in the mechanism of AV nodal facilitation. Atrial and His (H) bundle electrograms and microelectrode recordings from proximal AV nodal cells were analyzed in 15 superfused rabbit AV node preparations. The pacing protocol consisted of 30 basic beats (S1; coupling interval S1-S1= 300 ms) followed by a facilitating prematurity (S2; coupling intervals S1-S2of 300, 200, 150, and 130 ms) followed by the test beat (S3; coupling interval S2-S3scanned in 5-ms steps). Conduction curves (S2-H2vs. S1-S2, S3-H3vs. S2-S3, and S3-H3vs. H2-S3) were constructed. Facilitation (i.e., shortening of S3-H3when S1-S2was shortened) was demonstrated in all preparations using the H2-S3( P < 0.001) but not the S2-S3format. Microelectrode recordings revealed a causal relationship between the improved proximal AV nodal cellular responses in facilitation and the prolonged S2-S3interval. There was no evidence for enhanced nodal dromotropic function directly resulting from the introduction of the facilitating beats. Thus facilitation is based on inherent cycle-length-dependent properties of the AV node during application of a complex pacing protocol and primarily reflects the uncontrolled modulation of the proximal cellular response.

ROLE OF ACTION POTENTIAL SHORTENING IN THE PREVENTION OF ARRHYTHMIAS IN CANINE CARDIAC TISSUE

1999 ◽  
Vol 26 (12) ◽  
pp. 964-969 ◽  
Author(s):  
Kawonia P Mull ◽  
Qadriyyah Debnam ◽  
Syeda M Kabir ◽  
Mohit Lal Bhattacharyya
Keyword(s):  
Action Potential ◽  
Cardiac Tissue ◽  
Action Potential Shortening

Acetate-induced depression of electrical and contractile activity in normoxic and hypoxic guinea pig papillary muscle

1989 ◽  
Vol 67 (7) ◽  
pp. 734-739
Author(s):  
Hideharu Hayashi ◽  
Hajime Terada ◽  
Alexander Kholopov ◽  
Terence F. McDonald
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Action Potential Duration ◽  
Contractile Activity ◽  
High Energy ◽  
Factors Affecting ◽  
Resting Tension ◽  
Tension Increase ◽  
Action Potential Shortening ◽  
Action Potential Configuration

The action potential configuration, developed tension, and resting tension were monitored in normoxic and hypoxic guinea pig papillary muscles superfused with solutions containing no substrate, glucose, or acetate (1–10 mM). In normoxic muscle, acetate provoked a concentration-dependent transient depression of the action potential duration and force of contraction, depression was maximal after 10–30 min, and recovery was complete after 90–120 min. In hypoxic muscle, acetate accelerated functional rundown (action potential shortening, decline of developed tension, increase in resting tension). Because rundown in hypoxic muscle was sensitive to factors affecting glycolysis (moderated by external glucose; accentuated by 2-deoxyglucose), the accentuated rundown with acetate may be accounted for by a partial block of glycolysis. However, block of glycolysis cannot explain the acetate-induced transient depression in normoxic muscle, since the depression was enhanced in normoxic muscle with 2-deoxyglucose-blocked glycolysis. We suggest that the transient depression is due to a transient depression of high energy nucleotides with consequent effects on ionic currents.Key words: acetate, action potential duration, 2-deoxyglucose, hypoxia, ATP.

scholarly journals Effects of Volatile Anesthetics on Atrial and AV Nodal Electrophysiological Properties in Guinea Pig Isolated Perfused Heart 

1998 ◽  
Vol 89 (2) ◽  
pp. 434-442 ◽  
Author(s):  
Pekka M. J. Raatikainen ◽  
Mark F. Trankina ◽  
Timothy E. Morey ◽  
Donn M. Dennis
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Action Potential Duration ◽  
Volatile Anesthetics ◽  
Monophasic Action Potential ◽  
Computer Assisted ◽  
Conduction Time ◽  
Av Node ◽  
Refractory Periods ◽  
Supraventricular Tachycardias

Background Knowledge of the anesthetic effects on atrial and atrioventricular (AV) nodal electrophysiologic properties is fundamental to understand the modulatory role of anesthetics on the pathogenesis of supraventricular tachycardias, and to individualize the perioperative management of patients with supraventricular tachycardias or AV nodal conduction disturbances. Therefore the authors studied the effects of three commonly used volatile anesthetics on the electrophysiologic properties of the atrium and AV node. Methods The concentration-dependent electrophysiologic effects of halothane, isoflurane, and desflurane (0-2 minimum alveolar concentration [MAC]) were studied in guinea pig Langendorff-perfused hearts fit with instruments to simultaneously measure atrial and AV nodal conduction times and atrial monophasic action potential duration. Atrial and AV nodal effective refractory periods were measured simultaneously using a computer-assisted premature stimulation protocol. The concentrations of anesthetics in the gas phase were monitored by an infrared gas analyzer. Results Volatile anesthetics caused markedly different concentration-dependent effects on atrial conduction, repolarization, and refractoriness, and on AV nodal function. At equianesthetic concentrations, halothane depressed atrial conduction the most, whereas desflurane caused the greatest shortening of atrial monophasic action potential duration. Halothane had no significant effect on atrial refractoriness, whereas at 2 MAC desflurane significantly shortened and isoflurane significantly prolonged atrial effective refractory periods by 18.1+/-13.5% and 13.2+/-14.7%, respectively. On an equi-MAC basis, the rank order of potency for the anesthetics to prolong AV nodal conduction time and AV nodal ERP was halothane &gt; desflurane &gt; isoflurane. Conclusion The different electrophysiologic effects of volatile anesthetics in the atrium and AV node suggest that these agents may modulate atrial dysrhythmogenesis in distinctly different ways.

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