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1 Biomedical Engineering, Washington University, Saint Louis, Missouri, United States
2 Biomedical Engineering, Washington University, Saint Louis, Missouri, United States; University of Manchester, Manchester, United Kingdom
3 Cardiology Research Center, Moscow, Russian Federation
* To whom correspondence should be addressed. E-mail: igor{at}wustl.edu.
Vagal stimulation results in complex changes of pacemaker excitability in the sinoatrial node (SAN). To investigate the vagal effects in rabbit SAN, we used optical mapping, which is the only technology that allows resolving simultaneously changes in activation pattern and action potentials morphologies. We identified by immunolabeling the SAN as neurofilament 160 positive, but connexin 43 negative region (n=5). Normal excitation originated in the SAN center with a cycle length (CL) of 405±14 ms (n=10), spread anisotropically along the crista terminalis (CT), and failed to conduct toward the septum. Postganglionic nerve stimulation (PNS, 400-800ms) reduced CL by 74±7% transiently and shifted the leading pacemaker inferiorly (78%) or superiorly (22%) from the SAN center by 2-10mm. In the intercaval region between the SAN center and the septal block zone, PNS produced an 8±1mm2 region of transient hyperpolarization and inexcitability. The first spontaneous or paced excitation following PNS could not enter this region for 500-1500ms. Immunolabeling revealed that the PNS-induced inexcitable region is located between the SAN center and the block zone, and has a 2.5-fold higher density of choline acetyltransferase (ChAT) than CT but 3-fold lower than SAN center. The fact that the inexcitability region does not coincide with the most innervated area, indicates that the properties of the myocytes themselves, as well as intercellular coupling, must play a role in the inexcitability induction. Conclusions: Optically mapping revealed that PNS resulted in transient loss of pacemaker cell excitability and unidirectional entrance conduction block in the periphery of SAN.
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