| Vagally induced depression of impulse propagation as a cause of atrial tachycardia. | |
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MedLine Citation:
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PMID: 2038074 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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It is known that parasympathetic influence favors induction of re-entrant atrial tachycardias (ATs). This effect is usually interpreted as a result of inhomogeneous shortening of atrial refractoriness leading to increased probability of circus movement following a premature impulse. However, early microelectrode studies showed that in spontaneously beating isolated frog atria, intensive vagal stimulation (VS) induced paroxysms of rapid AT in the absence of myocardial extrastimulation. This AT was found to correlate with inexcitability of some of the impaled fibers of the atria. It was supposed that temporary, vagally induced, inexcitable areas of the atria could lead to re-entry, serving as a site of unidirectional conduction. This hypothesis was recently evaluated by direct multielectrode mapping of excitation sequence during vagally induced AT in frog atria. Recording from 32 sites with a spatial resolution of 1-2 mm clearly showed that the AT was due to re-entry. The ATs were always preceded by vagally induced depression of conduction, with some areas of the atria being completely blocked. As the vagal influence decreased, the blocked areas recovered in an inhomogeneous manner. The re-entrant AT was initiated when a sinus impulse arrived during a certain phase of the recovery. Unlike the well-known mechanism of re-entry, which is based on inhomogeneous refractoriness and extrabeat(s), the re-entrant AT in our model depended on vagally induced conduction block and could be launched by a single sinus impulse. |
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Authors:
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L V Rosenshtraukh; A V Zaitsev; V G Fast; A M Pertsov; V I Krinsky |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Journal of molecular and cellular cardiology Volume: 23 Suppl 1 ISSN: 0022-2828 ISO Abbreviation: J. Mol. Cell. Cardiol. Publication Date: 1991 Feb |
Date Detail:
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Created Date: 1991-07-03 Completed Date: 1991-07-03 Revised Date: 2003-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0262322 Medline TA: J Mol Cell Cardiol Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 3-9 Citation Subset: IM |
Affiliation:
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Institute of Experimental Cardiology, All-Union Cardiology Research Center, Moscow, USSR. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Electric Conductivity Heart Atria / innervation, physiopathology Microelectrodes Neural Conduction Rana temporaria Tachycardia / etiology* Vagus Nerve / physiopathology* |
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