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.

Images of Action Potential Propagation in Heart

Physiology ◽  
2000 ◽  
Vol 15 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Guy Salama ◽  
Bum-Rak Choi
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Imaging Techniques ◽  
Three Dimensional ◽  
Fiber Structure ◽  
Intercellular Coupling ◽  
Av Node ◽  
Action Potential Propagation ◽  
Voltage Sensitive Dyes

Activation and repolarization across mammalian hearts follow complex three-dimensional pathways that are governed by fiber structure, intercellular coupling, and action potentials (APs) with spatially heterogeneous properties. Voltage-sensitive dyes and imaging techniques offer new insights on how spatiotemporal heterogeneities of APs govern propagation, repolarization, and AV node conduction and help us visualize arrhythmias with previously unattainable details.

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.

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.

Abstract MP083: Autonomic Imbalance at the Level of Atrioventricular Node, but Not at the Level of Sinus Node, is Associated With Sudden Cardiac Death: The Atherosclerosis Risk in Community Study

Circulation ◽  
2017 ◽  
Vol 135 (suppl_1) ◽  
Author(s):  
Srini V Mukundan ◽  
Muammar M Kabir ◽  
Jason Thomas ◽  
Golriz Sedaghat ◽  
Jonathan W Waks ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Cox Regression ◽  
Sinus Node ◽  
Atrioventricular Node ◽  
Av Node ◽  
Atherosclerosis Risk In Communities ◽  
Autonomic Imbalance ◽  
Summary Effect ◽  
Atherosclerosis Risk

Introduction: Autonomic imbalance, quantified by decreased heart rate variability (HRV), is associated with increased cardiovascular mortality. It is unknown if autonomic influences on sinus and atrioventricular (AV) nodes are equally important for the risk of sudden cardiac death (SCD). Hypothesis: Autonomic influences on sinus and AV node are equally strongly associated with increased SCD, non-sudden cardiac death (non-SCD), and non-cardiac death. Methods: Baseline visit 10-second ECGs (n=14,250) of the Atherosclerosis Risk in Communities (ARIC) cohort were analyzed. Normalized variance of P-onset to P-onset intervals (PPVN) and QRS-onset to QRS-onset intervals (QQVN) was calculated to assess autonomic influence on sinus and AV node respectively. Normalized variance of Rpeak - Rpeak intervals was determined as HRV measure. Values were log-transformed to normalize distribution. SCD served as primary outcome. Secondary outcomes were non-SCD and non-cardiac death. Three Cox regression models were constructed for dichotomized at 20 th percentile predictor variables. Results: Over median follow-up of 24.4 years, there were 497 SCDs (incidence 1.66 [95%CI 1.52-1.82], 742 non-SCDs (incidence 2.48 [95%CI 2.31-2.67], and 3,753 non-cardiac deaths (incidence 12.6 [95%CI 12.1-13.0]) per 1,000 person-years. In paired analysis, LogPPVN was significantly larger than LogQQVN (-7.28±1.06 vs. -7.72±1.24; P<0.0001). There was no difference between LogQQVN and Log RRVN (-7.72±1.24 vs -7.72±1.23; P=0.364). After full adjustment, LogRRVN and LogQQVN were significantly associated with non-SCD and SCD. Association with non-SCD was stronger. LogPPVN was independently associated with non-SCD but not SCD. No value was associated with non-cardiac death. Conclusion: Autonomic imbalance at the AV node, with likely summary effect at the bundle of His, is associated with SCD and non-SCD. Autonomic imbalance at the SA node is associated with non-SCD only. Autonomic input to SA and AV node should be further studied.

Acetylcholine lengthens action potentials of sheep cardiac Purkinje fibers

1980 ◽  
Vol 238 (2) ◽  
pp. H237-H243
Author(s):  
S. L. Lipsius ◽  
W. R. Gibbons
Keyword(s):  
Muscarinic Receptors ◽  
Action Potential Duration ◽  
Action Potentials ◽  
Purkinje Fibers ◽  
Diastolic Depolarization ◽  
Cardiac Purkinje Fibers ◽  
Rate Of Increase ◽  
Definite Sequence ◽  
Microelectrode Techniques ◽  
Diastolic Potential

The effect of acetylcholine (ACh) on the electrical activity of sheep cardiac Purkinje fibers was studied using standard microelectrode techniques. Most fibers showed a definite sequence of changes when exposed to ACh. Initially, action potential duration (APD) increased markedly. After about 20 s, the maximum diastolic potential (MDP) started to become more negative and, at the same time, the rate of increase in APD slowed. Once the MDP stabilized at a more negative level, the APD usually resumed its rapid increase. ACh also increased the slope of diastolic depolarization and made the plateau voltage more positive. APD was increased by ACh concentrations as low as 10(-7) M, and it increased with concentrations up to 10(-5) M (the highest concentration tested). ACh-induced increases in APD depended on the stimulation frequency; 2-min exposures to 10(-6) M ACh increased APD by 76.8 +/- 14.7% at 6 min-1 and 17.7 +/- 4.2% at 60 min-1. Atropine blocked all the effects of ACh. Hexamethonium did not prevent the ACh effects. It is concluded that ACh acts via muscarinic receptors. The changes in APD and MDP appear to be separate events, and it is difficult to see how the former effect may be explained by known actions of ACh.

scholarly journals MyoR Modulates Cardiac Conduction by Repressing Gata4

2014 ◽  
Vol 35 (4) ◽  
pp. 649-661 ◽  
Author(s):  
John P. Harris ◽  
Minoti Bhakta ◽  
Svetlana Bezprozvannaya ◽  
Lin Wang ◽  
Christina Lubczyk ◽  
...  
Keyword(s):  
Transcriptional Repression ◽  
Atrioventricular Node ◽  
Electrical Activation ◽  
Cardiac Conduction ◽  
Specific Gene ◽  
Dependent Manner ◽  
Regulatory Circuit ◽  
Genetic Deletion ◽  
Repression Domain ◽  
Av Delay

The cardiac conduction system coordinates electrical activation through a series of interconnected structures, including the atrioventricular node (AVN), the central connection point that delays impulse propagation to optimize cardiac performance. Although recent studies have uncovered important molecular details of AVN formation, relatively little is known about the transcriptional mechanisms that regulate AV delay, the primary function of the mature AVN. We identify here MyoR as a novel transcription factor expressed in Cx30.2+cells of the AVN. We show that MyoR specifically inhibits a Cx30.2 enhancer required for AVN-specific gene expression. Furthermore, we demonstrate that MyoR interacts directly with Gata4 to mediate transcriptional repression. Our studies reveal that MyoR contains two nonequivalent repression domains. While the MyoR C-terminal repression domain inhibits transcription in a context-dependent manner, the N-terminal repression domain can function in a heterologous context to convert the Hand2 activator into a repressor. In addition, we show that genetic deletion of MyoR in mice increases Cx30.2 expression by 50% and prolongs AV delay by 13%. Taken together, we conclude that MyoR modulates a Gata4-dependent regulatory circuit that establishes proper AV delay, and these findings may have wider implications for the variability of cardiac rhythm observed in the general population.

A System of Electrically Coupled Small Cells in the Buccal Ganglia of the Pond Snail Planorbis Corneus

1972 ◽  
Vol 56 (3) ◽  
pp. 621-637
Author(s):  
MICHAEL S. BERRY
Keyword(s):  
Synaptic Input ◽  
Action Potentials ◽  
Burst Activity ◽  
Small Cells ◽  
Pond Snail ◽  
Trigger System ◽  
Buccal Ganglia ◽  
Large Numbers ◽  
Planorbis Corneus

1. The buccal ganglia of Planorbis contain a population of electrically coupled small cells. This has been studied, in preparations of isolated ganglia, by recording intracellularly from the cells two at a time. 2. The population is usually silent but activity initiated in any one of its members tends to spread to the rest of the population in both ganglia. Failure of spread, or fatigue, gradually occurs on repetition. 3. The group has the properties of a trigger system, initiating prolonged patterned activity in large numbers of neurones in the buccal ganglia. This may normally initiate feeding. 4. In addition to central processes, both in the buccal ganglia and to the rest of the CNS, the system has peripheral axons in most of the buccal nerves. No synaptic input could be demonstrated. 5. Action potentials in some of the cells increase greatly in duration with repetition. The resulting electrotonic EPSP's, recorded in closely coupled trigger cells, correspondingly increase in size. The possible integrative significance of this is discussed, especially its effect in offsetting fatigue. 6. In some preparations spontaneous bursting occurred in trigger cells and this elicited burst activity in large neurones, including motoneurones. The system may have an intrinsic pacemaker.

Anatomy and physiology of the atrioventricular node

ESC CardioMed ◽  
2018 ◽  
pp. 1957-1958
Author(s):  
M. J. Pekka Raatikainen
Keyword(s):  
Atrioventricular Node ◽  
Cardiac Conduction ◽  
Ventricular Rate ◽  
Pacemaker Activity ◽  
Av Block ◽  
Anatomy And Physiology ◽  
Specialized Tissue ◽  
Crucial Part ◽  
Decremental Conduction ◽  
Sinoatrial Node Dysfunction

The atrioventricular node (AVN) and the surrounding area is a crucial part of the cardiac conduction system. It consists of specialized tissue located at the base of the atrial septum within the triangle of Koch. The inherent physiological function of the AVN is to delay cardiac impulse propagation between the atria and the ventricles, and to function as a backup pacemaker in the setting of sinoatrial node dysfunction or advanced atrioventricular (AV) block. AV nodal conduction and pacemaker activity are under strict control by the autonomic nervous system. Due to the unique property of decremental conduction, the AVN protects the heart from an excessive ventricular rate during rapid atrial arrhythmias. On the other hand, the AVN is also an important source of brady- and tachyarrhythmias, and a target for various pharmacological and non-pharmacological arrhythmia therapies.

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