Histamine and pacemaker shift in the sinoatrial node

1994 ◽  
Vol 41 (S1) ◽  
pp. C87-C88 ◽  
Author(s):  
E. Kevelaitis ◽  
R. Abraitis ◽  
R. Lazhauskas
Keyword(s):  
Sinoatrial Node ◽  
Pacemaker Shift

Computer simulations of pacemaker shift in the sinoatrial node

BIOPHYSICS ◽  
2010 ◽  
Vol 55 (6) ◽  
pp. 1025-1029 ◽  
Author(s):  
R. A. Syunyaev ◽  
R. R. Aliev
Keyword(s):  
Computer Simulations ◽  
Sinoatrial Node ◽  
Pacemaker Shift

Investigation of pacemaker shift in the rabbit sinoatrial node using the optical mapping technique

BIOPHYSICS ◽  
2010 ◽  
Vol 55 (3) ◽  
pp. 442-446
Author(s):  
D. V. Abramochkin ◽  
V. S. Kuzmin ◽  
G. S. Sukhova ◽  
L. V. Rosenshtraukh
Keyword(s):  
Sinoatrial Node ◽  
Optical Mapping ◽  
Mapping Technique ◽  
Pacemaker Shift ◽  
Rabbit Sinoatrial Node

Downward gradient in action potential duration along conduction path in and around the sinoatrial node

1999 ◽  
Vol 276 (2) ◽  
pp. H686-H698 ◽  
Author(s):  
M. R. Boyett ◽  
H. Honjo ◽  
M. Yamamoto ◽  
M. R. Nikmaram ◽  
R. Niwa ◽  
...  
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Sinoatrial Node ◽  
Pacemaker Activity ◽  
Similar Data ◽  
Conduction Path ◽  
Crista Terminalis ◽  
Conduction Pathway ◽  
Pacemaker Shift ◽  
Rabbit Sinoatrial Node

Regional differences in electrical activity in rabbit sinoatrial node have been investigated by recording action potentials throughout the intact node or from small balls of tissue from different regions. In the intact node, action potential duration was greatest at or close to the leading pacemaker and declined markedly in all directions from it, e.g., by 74 ± 4% (mean ± SE, n = 4) to the crista terminalis. Similar data were obtained from the small balls. The gradient is down the conduction pathway and will help prevent reentry. In the intact node, a zone of inexcitable tissue with small depolarizations of <25 mV or stable resting potentials was discovered in the inferior part of the node, and this will again help prevent reentry. The intrinsic pacemaker activity of the small balls was slower in tissue from more inferior (as well as more central) parts of the node [e.g., cycle length increased from 339 ± 13 ms ( n = 6) to 483 ± 13 ms ( n = 6) in transitional tissue from more superior and inferior sites], and this may help explain pacemaker shift.

scholarly journals Pacemaker Shift in the Rabbit Sinoatrial Node in Response to Vagal Nerve Stimulation

2001 ◽  
Vol 86 (2) ◽  
pp. 177-184 ◽  
Author(s):  
Nitaro Shibata ◽  
Shin Inada ◽  
Kazuyuki Mitsui ◽  
Haruo Honjo ◽  
Mitsuru Yamamoto ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Sinoatrial Node ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Pacemaker Shift ◽  
Rabbit Sinoatrial Node

scholarly journals Assembly of the Cardiac Pacemaking Complex: Electrogenic Principles of Sinoatrial Node Morphogenesis

2021 ◽  
Vol 8 (4) ◽  
pp. 40
Author(s):  
Marietta Easterling ◽  
Simone Rossi ◽  
Anthony J Mazzella ◽  
Michael Bressan
Keyword(s):  
Cardiac Tissue ◽  
Sinoatrial Node ◽  
Cardiac Pacemaker ◽  
Tissue Level ◽  
Rhythmic Contraction ◽  
Entire Volume ◽  
Impulse Generation ◽  
Cardiac Pacemaking ◽  
Electrical Impulses ◽  
Sufficient Strength

Cardiac pacemaker cells located in the sinoatrial node initiate the electrical impulses that drive rhythmic contraction of the heart. The sinoatrial node accounts for only a small proportion of the total mass of the heart yet must produce a stimulus of sufficient strength to stimulate the entire volume of downstream cardiac tissue. This requires balancing a delicate set of electrical interactions both within the sinoatrial node and with the downstream working myocardium. Understanding the fundamental features of these interactions is critical for defining vulnerabilities that arise in human arrhythmic disease and may provide insight towards the design and implementation of the next generation of potential cellular-based cardiac therapeutics. Here, we discuss physiological conditions that influence electrical impulse generation and propagation in the sinoatrial node and describe developmental events that construct the tissue-level architecture that appears necessary for sinoatrial node function.

scholarly journals Intracellular Na+ Modulates Pacemaking Activity in Murine Sinoatrial Node Myocytes: An In Silico Analysis

2021 ◽  
Vol 22 (11) ◽  
pp. 5645
Author(s):  
Stefano Morotti ◽  
Haibo Ni ◽  
Colin H. Peters ◽  
Christian Rickert ◽  
Ameneh Asgari-Targhi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Membrane Potential ◽  
In Silico ◽  
Sinoatrial Node ◽  
In Silico Analysis ◽  
Ankyrin B ◽  
Deficient Mice ◽  
Silico Analysis ◽  
Bursting Activity

Background: The mechanisms underlying dysfunction in the sinoatrial node (SAN), the heart’s primary pacemaker, are incompletely understood. Electrical and Ca2+-handling remodeling have been implicated in SAN dysfunction associated with heart failure, aging, and diabetes. Cardiomyocyte [Na+]i is also elevated in these diseases, where it contributes to arrhythmogenesis. Here, we sought to investigate the largely unexplored role of Na+ homeostasis in SAN pacemaking and test whether [Na+]i dysregulation may contribute to SAN dysfunction. Methods: We developed a dataset-specific computational model of the murine SAN myocyte and simulated alterations in the major processes of Na+ entry (Na+/Ca2+ exchanger, NCX) and removal (Na+/K+ ATPase, NKA). Results: We found that changes in intracellular Na+ homeostatic processes dynamically regulate SAN electrophysiology. Mild reductions in NKA and NCX function increase myocyte firing rate, whereas a stronger reduction causes bursting activity and loss of automaticity. These pathologic phenotypes mimic those observed experimentally in NCX- and ankyrin-B-deficient mice due to altered feedback between the Ca2+ and membrane potential clocks underlying SAN firing. Conclusions: Our study generates new testable predictions and insight linking Na+ homeostasis to Ca2+ handling and membrane potential dynamics in SAN myocytes that may advance our understanding of SAN (dys)function.

scholarly journals Phase resetting in central and peripheral sinoatrial node cell models

2005 ◽  
Author(s):  
D.G. Tsalikakis ◽  
H.G. Zhang ◽  
D.I. Fotiadis ◽  
G.P. Kremmydas
Keyword(s):  
Sinoatrial Node ◽  
Phase Resetting ◽  
Cell Models ◽  
Sinoatrial Node Cell
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