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Functional and structural optical imagining of the rabbit sinoatrial node
Author(s) -
Fedorov Vadim V,
Hucker William J,
Dobrzynski Halina,
Efimov Igor R
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1304-c
It is commonly accepted that the cardiac impulse originates in a relatively small group of primary pacemaker cells in the central part of the sinoatrial node (SAN). However, animal and human studies have shown that under normal physiological conditions, the heart beat can originate in different leading pacemaker sites (LPS) within and outside of the SAN. In this study, we optically mapped the activation pattern of rabbit SAN preparations by fluorescent imaging. The SAN preparations (n=15) consisted of the right atrium, superior and inferior vena cava (SVC and IVC) regions, and atrial septum. We observed the “classic” position of the LPS in only 10 preparations; in another 3 we observed the LPS near the SVC and in the remaining 2 near the IVC. In addition, in two experiments we observed bi‐focal activation. The spontaneous cycle length in all preparations was 405±14 ms. From the LPS, activation spread along the atrial muscle of the crista terminalis (CT) in both SVC and IVC directions with a fast conduction velocity, but slowly spread perpendicular to the CT and was blocked in the region between the SAN and septum in all 15 preparations. The maximum conduction velocity was observed in the direction of fiber orientation, as determined by optical coherence tomography. Immunofluorescent microscopy with α‐actinin, connexin 43, neurofilament 160, and vimentin revealed that the block zone predominantly consists of fibroblasts. We conclude that nearly all pacemaker cells in the intercaval region can play a role as the LPS. We also confirmed our hypothesis that the block zone may be simply explained by absence or reduced number of myocytes. Supported by NIH grant HL58808

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