Effect of epinephrine on automaticity of the canine atrioventricular node

1975 ◽  
Vol 229 (1) ◽  
pp. 34-37 ◽  
Author(s):  
WW Tse
Keyword(s):  
Action Potentials ◽  
Present Experiment ◽  
Atrioventricular Node ◽  
Smooth Transition ◽  
Av Node ◽  
Single Fibers ◽  
His Bundle ◽  
Transmembrane Potentials ◽  
Spontaneous Rate ◽  
Microelectrode Techniques

Effects of epinephrine on the automaticity of canine AV nodal fibers were studied on spontaneously beating AV node-His bundle preparations. Transmembrane potentials of single fibers of the AV node or His bundle were recorded with microelectrode techniques. Action potentials of most AV nodal fibers were characterized by steep phase-4 depolarization and smooth transition from phases 4 to 0. Epinephrine (0.1-0.2 mug/ml) increased the spontaneous rate of the AV nodal fibers. The slope of phase 4 depolarization was increased and the threshold shifted to a more negative level. These changes probably accounted for the increase in the automaticity of the node. Also, in the presence of epinephrine, the pacemaker of the preparation was consistently located at the AV node had a higher degree of automaticity than the His bundle. The findings of the present experiment, therefore, further support the view that the AV node is automatic.

Adrenergic potentiation on spontaneous activity of canine paranodal fibers

1984 ◽  
Vol 247 (3) ◽  
pp. H415-H421
Author(s):  
W. W. Tse
Keyword(s):  
Spontaneous Activity ◽  
Tricuspid Valve ◽  
Action Potentials ◽  
Smooth Transition ◽  
Convex Side ◽  
Av Node ◽  
Junctional Tachycardia ◽  
His Bundle ◽  
Spontaneous Rate

The present study, using in vitro preparations, was designed to determine the anatomic, histological, and automatic properties of canine paranodal fibers. This tissue, together with the atrioventricular (AV) node and His bundle, constituted the three major tissues in the AV junction. The fascicles of the paranodal fibers ran parallel and adjacent to the base of the septal cusp of the tricuspid valve. The distal end of the paranodal fibers joined the lower half of the compact AV node on its convex side. Paranodal fibers when isolated were able to initiate spontaneous activity. Action potentials of many of these fibers showed primary pacemaker characteristics, i.e., a prominent phase 4 depolarization and smooth transition from phases 4 to 0. In 14 preparations, epinephrine (2.0 micrograms injected into the tissue bath) potentiated spontaneous rates to 144 +/- 6.0 beats/min from 61 +/- 5.0, an increase of 136%. Also, under the influence of epinephrine, paranodal fibers consistently generated a spontaneous rate higher than that of the AV node or His bundle, whether they were functionally connected or separated. These findings provide a basis for explaining the junctional tachycardia that occurs under adrenergic influence and demonstrate the presence of three major automatic tissues: the paranodal fibers, AV node, and His bundle in the canine AV junction.

Optical mapping of atrioventricular node reveals a conduction barrier between atrial and nodal cells

1998 ◽  
Vol 274 (3) ◽  
pp. H829-H845 ◽  
Author(s):  
Bum-Rak Choi ◽  
Guy Salama
Keyword(s):  
Action Potentials ◽  
Imaging Techniques ◽  
Atrioventricular Node ◽  
Small Cells ◽  
Av Node ◽  
Propagation Pattern ◽  
Voltage Sensitive Dyes ◽  
Decremental Conduction ◽  
Microelectrode Techniques ◽  
Av Delay

The mechanisms responsible for atrioventricular (AV) delay remain unclear, in part due to the inability to map electrical activity by conventional microelectrode techniques. In this study, voltage-sensitive dyes and imaging techniques were refined to detect action potentials (APs) from the small cells comprising the AV node and to map activation from the “compact” node. Optical APs (124) were recorded from 5 × 5 mm (∼0.5-mm depth) AV zones of perfused rabbit hearts stained with a voltage-sensitive dye. Signals from the node exhibited a set of three spikes; the first and third ( peaks I and III) were coincident with atrial (A) and ventricular (V) electrograms, respectively. The second spike ( peak II) represented the firing of midnodal (N) and/or lower nodal (NH) cell APs as indicated by their small amplitude, propagation pattern, location determined from superimposition of activation maps and histological sections of the node region, dependence on depth of focus, and insensitivity to tetrodotoxin (TTX). AV delays consisted of τ1 (49.5 ± 6.59 ms, 300-ms cycle length), the interval between peaks I and II (perhaps AN to N cells), and τ2 (57.57 ± 5.15 ms), the interval between peaks II and III (N to V cells). The conductance time across the node was 10.33 ± 3.21 ms, indicating an apparent conduction velocity (ΘN) of 0.162 ± 0.02 m/s ( n = 9) that was insensitive to TTX. In contrast, τ1 correlated with changes in AV node delays (measured with surface electrodes) caused by changes in heart rate or perfusion with acetylcholine. The data provide the first maps of activation across the AV node and demonstrate that ΘN is faster than previously presumed. These findings are inconsistent with theories of decremental conduction and prove the existence of a conduction barrier between the atrium and the AV node that is an important determinant of AV node delay.

Letters to the Editor

1998 ◽  
Vol 275 (5) ◽  
pp. H1905-H1909 ◽  
Author(s):  
Igor R. Efimov
Keyword(s):  
Imaging Techniques ◽  
Atrioventricular Node ◽  
Small Cells ◽  
Letters To The Editor ◽  
Av Node ◽  
Propagation Pattern ◽  
Voltage Sensitive Dyes ◽  
Decremental Conduction ◽  
Microelectrode Techniques ◽  
Av Delay

The following is an abstract of the article discussed in the subsequent letter:  Choi, Bum-Rak, and Guy Salama. Optical mapping of atrioventricular node reveals a conduction barrier between atrial and nodal cells. Am. J. Physiol. 274 ( Heart Circ. Physiol. 43): H829–H845, 1998.—The mechanisms responsible for atrioventricular (AV) delay remain unclear, in part due to the inability to map electrical activity by conventional microelectrode techniques. In this study, voltage-sensitive dyes and imaging techniques were refined to detect action potentials (APs) from the small cells comprising the AV node and to map activation from the “compact” node. Optical APs (124) were recorded from 5 × 5 mm (∼0.5-mm depth) AV zones of perfused rabbit hearts stained with a voltage-sensitive dye. Signals from the node exhibited a set of three spikes; the first and third ( peaks Iand III) were coincident with atrial (A) and ventricular (V) electrograms, respectively. The second spike ( peak II)represented the firing of midnodal (N) and/or lower nodal (NH) cell APs as indicated by their small amplitude, propagation pattern, location determined from superimposition of activation maps and histological sections of the node region, dependence on depth of focus, and insensitivity to tetrodotoxin (TTX). AV delays consisted of τ1 (49.5 ± 6.59 ms, 300-ms cycle length), the interval between peaks I and II (perhaps AN to N cells), and τ2 (57.57 ± 5.15 ms), the interval between peaks II and III (N to V cells). The conductance time across the node was 10.33 ± 3.21 ms, indicating an apparent conduction velocity (ΘN) of 0.162 ± 0.02 m/s ( n = 9) that was insensitive to TTX. In contrast, τ1 correlated with changes in AV node delays (measured with surface electrodes) caused by changes in heart rate or perfusion with acetylcholine. The data provide the first maps of activation across the AV node and demonstrate that ΘN is faster than previously presumed. These findings are inconsistent with theories of decremental conduction and prove the existence of a conduction barrier between the atrium and the AV node that is an important determinant of AV node delay.

Atrioventricular nodal conduction during atrial fibrillation in rabbit heart

1982 ◽  
Vol 243 (5) ◽  
pp. H754-H760 ◽  
Author(s):  
T. Mazgalev ◽  
L. S. Dreifus ◽  
J. Bianchi ◽  
E. L. Michelson
Keyword(s):  
Atrial Fibrillation ◽  
Action Potentials ◽  
Atrioventricular Node ◽  
Interatrial Septum ◽  
Rabbit Heart ◽  
Relative Timing ◽  
Crista Terminalis ◽  
His Bundle ◽  
Atrioventricular Nodal Conduction ◽  
Variable Interaction

Atrial fibrillation was induced in 15 superfused rabbit atrial-atrioventricular nodal preparations in which surface bipolar electrograms were recorded simultaneously from the crista terminalis, interatrial septum, and His bundle along with microelectrode action potentials from cells in the atrionodal (AN), nodal (N), and nodal-His (NH) regions of the atrioventricular node. Effective engagement of the atrioventricular node with propagation to the His bundle was critically dependent on the relative timing of activation at the crista terminalis and interatrial septal input regions of the atrioventricular node. Conduction through the AN and N regions appeared dependent on the relative timing of activation wave fronts emerging from the two input regions. Asynchronous engagement of AN and N regions resulted in both distortion of action potentials and concealed conduction, with delayed conduction and block to the NH region and His bundle. Successful engagement of the NH region always produced a 1:1 NH-to-His bundle relationship. It is concluded that during atrial fibrillation 1) activation of the AN region occurs as a result of the variable interaction of inputs from the crista terminalis and interatrial septum; 2) predictably, effective synchronous engagement of the AN and consequently the N region is responsible for conduction to the NH and His bundle regions; 3) conversely, asynchronous activation inputs from the crista terminalis and interatrial septum result in fragmented, asynchronous as well as concealed conduction within the AN and N regions with block in the atrioventricular node and variable conduction to the His bundle.

Postextrasystolic Potentiation of Contraction in Cardiac Muscle

1956 ◽  
Vol 185 (1) ◽  
pp. 95-102 ◽  
Author(s):  
Brian F. Hoffman ◽  
Elliot Bindler ◽  
E. E. Suckling
Keyword(s):  
Right Ventricle ◽  
Action Potentials ◽  
Transmembrane Potential ◽  
Isometric Tension ◽  
Papillary Muscles ◽  
Postextrasystolic Potentiation ◽  
Single Fibers ◽  
Transmembrane Potentials ◽  
Diastolic Interval ◽  
The Right

The phenomenon of postextrasystolic potentiation of contraction has been studied in papillary muscles isolated from the right ventricle of dog and cat hearts. Isometric tension has been recorded by means of an electronic transducer (RCA #5734) and electrical activity of single fibers by means of an intracellular microelectrode. The degree of potentiation of contraction resulting from a single extrasystole is directly related to the degree of prematurity of this beat. Evidence has been obtained which indicates that the potentiation is maximally effective immediately after the extrasystole and decays at a progressively slower rate during the course of seven to ten beats. The appearance of postextrasystolic potentiation is not dependent upon the changes in frequency of contraction, diastolic interval or presystolic tension which result from the premature contraction. Studies of the transmembrane potentials of single fibers reveal no change in amplitude and little change in configuration of the action potentials associated with potentiated beats. Studies of the resting transmembrane potential and the effects of changes in extracellular concentrations of K and Ca fail to support the concept that potentiation is related solely to changes in the fiber K content. It is concluded that postextrasystolic potentiation results from mechanisms which remain unknown.

scholarly journals Can atrioventricular node ablation be safely performed in patients with permanent His bundle pacing? Data from a multicentric registry

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C Chaumont ◽  
N Auquier ◽  
A Mirolo ◽  
E Popescu ◽  
A Milhem ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Rate Control ◽  
Atrioventricular Node ◽  
Atrial Arrhythmia ◽  
Av Node ◽  
His Bundle ◽  
His Bundle Pacing ◽  
Ventricular Lead ◽  
Qrs Duration

Abstract Introduction Ventricular rate control is essential in the management of atrial fibrillation. Atrioventricular node ablation (AVNA) and ventricular pacing can be an effective option when pharmacological rate control is insufficient. However, right ventricular pacing (RVP) induces ventricular desynchronization in patients with normal QRS and increases the risk of heart failure on long term. His bundle pacing (HBP) is a physiological alternative to RVP. Observational studies have demonstrated the feasibility of HBP but there is still very limited data about the feasibility of AVNA after HBP. Purpose To evaluate feasibility and safety of HBP followed by AVNA in patients with non-controlled atrial arrhythmia. Methods We included in three hospitals between september 2017 and december 2019 all patients who underwent AVNA for non-controlled atrial arrhythmia after permanent His bundle pacing. No back-up right ventricular lead was implanted. AVNA procedures were performed with 8 mm-tip ablation catheter. Acute HBP threshold increase during AVNA was defined as a threshold elevation >1V. His bundle capture (HBC) thresholds were recorded at 3 months follow-up. Results AVNA after HBP lead implantation was performed in 45 patients. HBP and AVNA were performed simultaneously during the same procedure in 10. AVNA was successful in 32 of 45 patients (71%). Modulation of the AV node conduction was obtained in 7 patients (16%). The mean procedure duration was 42±24min, and mean fluoroscopy duration was 6.4±8min. A mean number of 7.7±9.9 RF applications (347±483 sec) were delivered to obtain complete / incomplete AV block. Acute HBC threshold increase occurred in 8 patients (18%) with return to baseline value at day 1 in 5 patients. There was no lead dislodgment during the AVNA procedures. Mean HBC threshold at implant was 1.26±[email protected] and slightly increased at 3 months follow-up (1.34±[email protected]). AV node re-conduction was observed in 5 patients (16% of the successful procedures) with a second successful ablation procedure in 4 patients. No ventricular lead revision was required during the follow-up period. The baseline native QRS duration was 102±21 ms and the paced QRS duration was 107±18 ms. Conclusion AVNA combined with HBP for non-controlled atrial arrhythmia is feasible and does not compromise HBC but seems technically difficult with significant AV nodal re-conduction rate. The presence of a back-up right ventricular lead could have changed our results and therefore would require further evaluation. Unipolar HBP after AV node ablation Funding Acknowledgement Type of funding source: None

Morphology and electrophysiology of the mammalian atrioventricular node

1988 ◽  
Vol 68 (2) ◽  
pp. 608-647 ◽  
Author(s):  
F. L. Meijler ◽  
M. J. Janse
Keyword(s):  
Mammalian Species ◽  
Conduction Block ◽  
Atrioventricular Node ◽  
Conduction Delay ◽  
Conduction Time ◽  
Av Node ◽  
Crista Terminalis ◽  
His Bundle ◽  
Transitional Cells ◽  
Av Bundle

The AV node of those mammalian species in which it has been thoroughly investigated (rabbit, ferret, and humans) consists of various cell types: transitional cells, midnodal (or typical nodal cells), lower nodal cells, and cells of the AV bundle. There are at least two inputs to the AV node, a posterior one via the crista terminalis and an anterior one via the interatrial septum, where atrial fibers gradually merge with transitional cells. The role of a possible third input from the left atrium has not been investigated. Since the transition from atrial fibers to nodal fibers is gradual, it is very difficult to define the "beginning" of the AV node, and gross measurements of AV nodal length may be misleading. Histologically, the "end" of the AV node is equally difficult to define. At the site where macroscopically the AV node ends, at the point where the AV bundle penetrates into the membranous septum, typical nodal cells intermingle with His bundle cells. A conspicuous feature, found in all species studied, is the paucity of junctional complexes, most marked in the midnodal area. The functional counterpart of this is an increased coupling resistance between nodal cells. An electrophysiological classification of the AV nodal area, based on transmembrane action potential characteristics during various imposed atrial rhythms (rapid pacing, trains of premature impulses), into AN (including ANCO and ANL), N, and NH zones has been described by various authors for the rabbit heart. In those studies in which activation patterns, transmembrane potential characteristics, and histology have been compared, a good correlation has been found between AN and transitional cells, N cells and the area where transitional cells and cells of the beginning of the AV bundle merge with midnodal cells, and NH cells and cells of the AV bundle. Dead-end pathways correspond to the posterior extension of the bundle of lower nodal cells and to anterior overlay fibers. During propagation of a normal sinus beat, activation of the AN zone accounts for at least 25% of conduction time from atrium to His bundle, the small N zone being the main source of AV nodal delay. Cycle length-dependent conduction delay is localized in the N zone. Conduction block of premature atrial impulses can occur both in the N zone and in the AN zone, depending on the degree of prematurity. Several factors determining AV nodal conduction delay have been identified.(ABSTRACT TRUNCATED AT 400 WORDS)

A method for isolating rabbit atrioventricular node myocytes which retain normal morphology and function

1993 ◽  
Vol 265 (2) ◽  
pp. H755-H766 ◽  
Author(s):  
J. C. Hancox ◽  
A. J. Levi ◽  
C. O. Lee ◽  
P. Heap
Keyword(s):  
Action Potentials ◽  
Sodium Current ◽  
Atrioventricular Node ◽  
Outward Current ◽  
Cellular Level ◽  
Isolation Procedure ◽  
Significant Advance ◽  
Av Node ◽  
Normal Morphology ◽  
Ventricular Cells

This report describes a method for isolating single rabbit atrioventricular (AV) node myocytes which retain their normal morphology when exposed to millimolar levels of calcium. Previous attempts to isolate cells from the AV node have produced myocytes that "round up" (i.e., go into contracture) when exposed to calcium. We show that the cells isolated with our technique possess properties similar to those described for intact AV nodal tissue. We find that single AV node myocytes are shorter and thinner (mean dimension = 103.5 +/- 2.3 by 7.8 +/- 0.2 microns; mean +/- SE, n = 90) than atrial or ventricular cells. Many of the cells produced by this isolation procedure generate spontaneous action potentials (188 +/- 9 beats/min; n = 6), which resemble action potentials recorded previously from the intact AV node. Voltage-clamp recordings from spontaneously active cells revealed similar membrane currents to those seen in intact tissue: fast sodium current and a L-type calcium current, followed by a delayed outward current. However, we found little evidence for the hyperpolarization-activated current (I(f)). Because the cells responded normally to concentrations of acetylcholine and isoproterenol within the physiological range, their cholinergic and adrenergic receptors appear to be well preserved by the isolation procedure. The ability to isolate morphologically and functionally normal AV myocytes may represent a significant advance for the investigation of nodal physiology at the cellular level.

The early development of the atrioventricular node and bundle of His in the embryonic chick heart. An electrophysiological and morphological study

Development ◽  
1988 ◽  
Vol 102 (3) ◽  
pp. 623-637
Author(s):  
C. Arguello ◽  
J. Alanis ◽  
B. Valenzuela
Keyword(s):  
Early Development ◽  
Action Potentials ◽  
Atrioventricular Node ◽  
Interatrial Septum ◽  
Embryonic Chick ◽  
Av Node ◽  
Cardiac Tissues ◽  
Electrical Recording ◽  
Chick Heart ◽  
Bundle Of His

The development of the atrioventricular node and bundle of His of embryonic chick hearts was studied by electrophysiological and morphological techniques. The dorsal wall of the AV canal and the interatrial septum were explored to determine if they contribute to the formation of the AV node and bundle of His. The resting membrane and action potentials of the interatrial septum cells were systematically analyzed and found to undergo progressive differentiation with development. The earliest identification of the AV node and upper bundle of His group of cells was achieved at 5 1/2–6 days of development by the electrical recording of their corresponding characteristic action potentials, from a circumscribed area located in the lowest and dorsal segment of the interatrial septum. The morphological and anatomical characterization of the cells was made following electrical recording and labelling with charcoal particles. The earlier AV node and bundle of His responses had similar characteristics to those of the adult heart. It is concluded that the AV node and upper bundle of His cells derive from the low interatrial septum. The possibility that AV canal cells contribute to this event was discarded. The functional relationship of the Av node and bundle of His with other cardiac tissues during the early development of the heart is discussed.

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