Action potentials alteration and arrhythmogenic conduction disturbances under alpha-1-adrenoreceptor activation in the murine pulmonary veinстатьяТезисы
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Дата последнего поиска статьи во внешних источниках: 14 августа 2017 г.
Аннотация:Study objectives: Recently, PV myocardium is considered as a main source for atrial fibrillation (AF) due to
spontaneous activity or re-entrant conduction of excitation. Adrenergic stimulation plays a central role in PVderived
AF. Nevertheless, the role of a-adrenoreceptor in PV arrhythmogenity remains poor understood. Thus,
the aim of the present study was to investigate the effects of a1 adrenoreceptor stimulation by phenylephrine
(Phe) on bioelectric activity and conduction in murine PV.
Methods: Mice (male, 20–30 g) were anaesthetized (urethane, 1.5 g/kg i.v.); multicellular preparations of left
atrium (LA) and PV were dissected and perfused at 37°C with Tyrode solution. Action potentials (AP) were
recorded in electrically paced preparations with use of standard microelectrode technique; duration of AP at 90%
repolarization (APD90%) was estimated. For excitation mapping and conduction velocity (CV) assessment, Tyrode-
perfused LA and PVs preparations were treated with potentially sensitive dye di-4-ANEPPS (5 lM).
Results: In part of experiments, Phe (10 lM) in both murine LA and PV reduced APD90%. However, in 50% of
PVs preparations, Phe significantly and rate dependently increased APD90%: to 114% (SS=200 ms) and to
164% (SS=80 ms) in respect to control level. Phe (10 lM) in both murine LA and PV significantly reduces CV.
This effect was more pronounced in PV myocardium. Conduction blocks and disturbances were observed in PV,
but not in LA, in the presence of Phe.
Conclusion: Phe induces arrythmogenic effects in murine PV. Murine PV experiments demonstrate that a1-adrenoreceptor
associated with arrhythmogenity may be caused by AP prolongation and conduction abnormalities.