Functional and morphological organization of the rabbit sinus node.

Bleeker, Wim K.; Mackaay, A. J. C.; Masson‐Pévet, Mireille; Bouman, L. N.; Becker, Axel

doi:10.1161/01.res.46.1.11

Cited by 339 publications

(281 citation statements)

References 31 publications

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“…T cells were long and spindle-shaped, diffusely distributing in the center and border of sinoatrial node area (Fig. 8A), which was consistent with earlier described data (2). Sinoatrial node cells in the FWC and the FPPP groups arranged disorderly and loosely, with obvious swelling, and the P cells could not be distinguished from T cells.…”

Section: Observation Of Sinoatrial Node Tissue and Cell Morphologysupporting

confidence: 91%

Comparative study between original and traditional method in establishing a chronic sinus node damage model in rabbit

Wang

et al. 2012

Journal of Applied Physiology

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L. Comparative study between original and traditional method in establishing a chronic sinus node damage model in rabbit. J Appl Physiol 113: 1802-1808, 2012. First published August 16, 2012 doi:10.1152/japplphysiol.00480.2012.-Sick Sinus Syndrome is a common and refractory arrhythmia, needing further study in which setting up a credible sinus node damage model is important. To explore the feasibility and superiority of an original formaldehyde pinpoint pressing permeation (FPPP) method for building a chronic sinus node damage (CSND) model, 5 rabbits were chosen from 35 as a sham-operation group, and the remaining were randomly divided into two groups: the formaldehyde wet compressing (FWC) group, in which models were established by applying a cotton bud dipped in 20% formaldehyde onto the sinus node (SN) area, and the FPPP group, in which models were established by injecting formaldehyde into the SN area through a self-made pinpointing and injecting electrode. We found that in both groups, the HR at 2 h, 24 h, 1 wk, and 2 wk after modeling decreased compared with premodeling; sinoatrial conduction time, sinus node recovery time, and corrected sinus node recovery time were prolonged compared with premodeling. The indexes mentioned shortened by 2 wk after modeling compared with 2 h in the FWC group, whereas they were stable after modeling in the FPPP group. The modeling achievement ratio in the FPPP group was higher and the death rate was lower. Under light microscope, paraffin sections of the SN tissue and cells showed severe injury in both groups. The results indicate that the CSND models in rabbits can be successfully established by the FPPP method, with higher achievement ratio, lower death rate, better stabilization effect, and less damaging comparing with the traditional method. chronic sinus node damage; model establishing; novel method; electrophysiology THE SICK SINUS SYNDROME (SSS) is a clinically common and refractory arrhythmia, whose precise pathogenesis has not yet been clearly elucidated. Clinical and experimental studies have shown that the cardiac pacing and conducting dysfunction resulting from the damage of sinus node (SN) cells may be the direct pathological mechanism (1). Therefore, the setting up of a credible and stable sinus node damage model is most important in the experimental study of SSS. Various methods are used to establish animal sinus node damage models. Most researchers utilize the method of applying a cotton bud dipped in 20% formaldehyde onto the sinus node area (6). Other methods include ligating the artery supplying the sinus node with blood (10), cryocoagulation of the sinus node area (4), and radiofrequency catheter ablation of the sinus node area (6). Most of these methods have difficulties pinpointing the sinus node area, require large incisal openings, and have a low survival rate. Moreover, they are only used to establish acute models rather than chronic ones. We therefore created a more refined approach, the formaldehyde pinpoint pressuring permeation (FPPP) method, f...

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Section: Observation Of Sinoatrial Node Tissue and Cell Morphologysupporting

confidence: 91%

Comparative study between original and traditional method in establishing a chronic sinus node damage model in rabbit

Wang

et al. 2012

Journal of Applied Physiology

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“…Earlier studies have shared our vision of initiation of true pacemaker activity that the pacemaker cycle begins with the DD acceleration. A detailed analysis of AP shapes in various regions of rabbit sinoatrial node revealed that the late acceleration of depolarization is observed as an earliest event within the pacemaker region [28]. Thus, intracellular Ca 2+ cycling provides primary (i.e.…”

Section: While Ion Channels Define Membrane Excitability They Do Notmentioning

confidence: 99%

Normal Heart Rhythm is Initiated and Regulated by an Intracellular Calcium Clock Within Pacemaker Cells

Maltsev

Lakatta

2007

Heart, Lung and Circulation

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For almost half a century it has been thought that the heart rhythm originates on the surface membrane of the cardiac pacemaker cells and is driven by voltage-gated ion channels (membrane clocks). Data from several recent studies, however, conclusively show that the rhythm is initiated, sustained, and regulated by oscillatory Ca 2+ releases (Ca 2+ clock) from the sarcoplasmic reticulum, a major Ca 2+ store within sinoatrial node cells, the primary heart's pacemakers. Activation of the local oscillatory Ca 2+ releases is independent of membrane depolarization and driven by a high level of basal state phosphorylation of Ca 2+ cycling proteins. The releases produce Ca 2+ wavelets under the cell surface membrane during the later phase of diastolic depolarization and activate the forward mode of Na + / Ca 2+ exchanger resulting in inward membrane current, which ignites an action potential. Phosphorylation-dependent gradation of speed at which Ca 2+ clock cycles is the essential regulatory mechanism of normal pacemaker rate and rhythm. The robust regulation of pacemaker function is insured by tight integration of Ca 2+ and membrane clocks: the action potential shape and ion fluxes are tuned by membrane clocks to sustain operation of the Ca 2+ clock which produces timely and powerful ignition of the membrane clocks to effect action potentials.

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“…The SA node is a spatially extended structure (Ϸ4ϫ5 mm in rabbit). 2 The leading pacemaker site is only Ϸ1% of the area of the SA node and is normally in the center of the SA node. 2 Normally, the periphery of the SA node serves to conduct the action potential from the center to the surrounding atrial muscle, although in various circumstances it can take over as the leading pacemaker site.…”

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confidence: 99%

“…2 The leading pacemaker site is only Ϸ1% of the area of the SA node and is normally in the center of the SA node. 2 Normally, the periphery of the SA node serves to conduct the action potential from the center to the surrounding atrial muscle, although in various circumstances it can take over as the leading pacemaker site. 3 The SA node is heterogeneous, and electrical activity changes from the periphery to the center in a characteristic fashion.…”

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confidence: 99%

“…3 The SA node is heterogeneous, and electrical activity changes from the periphery to the center in a characteristic fashion. 2 Cell size is known to decrease from the periphery to the center of the SA node, 2 and Honjo et al 4 reported that the electrical activity of single SA node cells from the rabbit is heterogeneous and changes from large to small cells in the same manner as from the periphery to the center of the SA node. These findings form the basis of the gradient model.…”

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confidence: 99%

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Gradient Model Versus Mosaic Model of the Sinoatrial Node

2001

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Background-A radical reinterpretation (mosaic model) of the makeup of the sinoatrial (SA) node has been proposed to explain the characteristic regional differences in electrical activity between the periphery and center of the SA node. According to the mosaic model, the differences result from a change in the mix of atrial cells and uniform SA node cells from periphery to center, whereas according to the alternative gradient model, there are no atrial cells within the functional SA node, and the differences result from a change in the intrinsic properties of SA node cells from periphery to center. Methods and Results-A mosaic model of peripheral and central tissue has been constructed computationally by use of a coupled ordinary differential equation network (CODE) in a 2D lattice (20ϫ20), with each node of the lattice designated randomly as an atrial cell or SA node cell (in correct proportions for periphery and center). The mosaic model fails to predict the characteristic differences in action potential rate and shape between the periphery and center, whereas the existing gradient model can do so. Conclusions-The mosaic model of the SA node is untenable, and the SA node is adequately described by the gradient model. (Circulation. 2001;103:584-588.)

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Functional and morphological organization of the rabbit sinus node.

Cited by 339 publications

References 31 publications

Comparative study between original and traditional method in establishing a chronic sinus node damage model in rabbit

Comparative study between original and traditional method in establishing a chronic sinus node damage model in rabbit

Normal Heart Rhythm is Initiated and Regulated by an Intracellular Calcium Clock Within Pacemaker Cells

Gradient Model Versus Mosaic Model of the Sinoatrial Node

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