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A Study of Mechanical Alternans in Single Rat Cardiomyocytes in Acetylcholine-CaCl2 Induced Atrial Fibrillation. / Mikhryakova, P. P.; Butova, X. A.; Myachina, T. A. и др.
в: Journal of Evolutionary Biochemistry and Physiology, Том 58, № S1, 2022, стр. S13-S21.

Результаты исследований: Вклад в журналСтатьяРецензирование

Harvard

Mikhryakova, PP, Butova, XA, Myachina, TA, Simonova, RA & Khokhlova, AD 2022, 'A Study of Mechanical Alternans in Single Rat Cardiomyocytes in Acetylcholine-CaCl2 Induced Atrial Fibrillation', Journal of Evolutionary Biochemistry and Physiology, Том. 58, № S1, стр. S13-S21. https://doi.org/10.1134/S002209302207002X

APA

Vancouver

Mikhryakova PP, Butova XA, Myachina TA, Simonova RA, Khokhlova AD. A Study of Mechanical Alternans in Single Rat Cardiomyocytes in Acetylcholine-CaCl2 Induced Atrial Fibrillation. Journal of Evolutionary Biochemistry and Physiology. 2022;58(S1):S13-S21. doi: 10.1134/S002209302207002X

Author

Mikhryakova, P. P. ; Butova, X. A. ; Myachina, T. A. и др. / A Study of Mechanical Alternans in Single Rat Cardiomyocytes in Acetylcholine-CaCl2 Induced Atrial Fibrillation. в: Journal of Evolutionary Biochemistry and Physiology. 2022 ; Том 58, № S1. стр. S13-S21.

BibTeX

@article{2cddd289090b491da8a7d4908ce04a24,
title = "A Study of Mechanical Alternans in Single Rat Cardiomyocytes in Acetylcholine-CaCl2 Induced Atrial Fibrillation",
abstract = "Atrial fibrillation (AF) is the most common cardiac arrhythmiaaccounting for significant morbidity and mortality. Cardiac alternans,defined at the cellular level as cyclic beat-to-beat alternationsin cell contraction, action potential morphology, and intracellularCa(2+) concentration, have been associatedwith sustained AF. Although alternans of action potential and intracellularCa(2+) transients in atrial cardiomyocytesin AF have been elucidated, little is known about the mechanicalalternans, cyclic alternations in contraction force, and cardiomyocyte shortening.Moreover, the susceptibility of different regions of atria to alternansformation is unclear. The aim of this study is to analyze and comparethe parameters of alternans in sarcomere shortening-relengtheningin single cardiomyocytes isolated from the left and right atria(LA, RA) of rats with acetylcholine-CaCl2 inducedAF. We found that autonomic AF provoked mechanical alternans insingle LA and RA cardiomyocytes. We also showed that the degreeand magnitude of mechanical alternans were greater in LA cardiomyocytesthan in RA cardiomyocytes. Our results propose that LA cardiomyocyteshave a greater susceptibility to AF-induced beat-to-beat alternans insarcomere shortening amplitudes than RA myocytes that may causeLA mechanical dysfunction.",
author = "Mikhryakova, {P. P.} and Butova, {X. A.} and Myachina, {T. A.} and Simonova, {R. A.} and Khokhlova, {A. D.}",
note = "This work was supported by the Russian Science Foundation no. 22-75-10134.",
year = "2022",
doi = "10.1134/S002209302207002X",
language = "English",
volume = "58",
pages = "S13--S21",
journal = "Journal of Evolutionary Biochemistry and Physiology",
issn = "0022-0930",
publisher = "Maik Nauka-Interperiodica Publishing",
number = "S1",

}

RIS

TY - JOUR

T1 - A Study of Mechanical Alternans in Single Rat Cardiomyocytes in Acetylcholine-CaCl2 Induced Atrial Fibrillation

AU - Mikhryakova, P. P.

AU - Butova, X. A.

AU - Myachina, T. A.

AU - Simonova, R. A.

AU - Khokhlova, A. D.

N1 - This work was supported by the Russian Science Foundation no. 22-75-10134.

PY - 2022

Y1 - 2022

N2 - Atrial fibrillation (AF) is the most common cardiac arrhythmiaaccounting for significant morbidity and mortality. Cardiac alternans,defined at the cellular level as cyclic beat-to-beat alternationsin cell contraction, action potential morphology, and intracellularCa(2+) concentration, have been associatedwith sustained AF. Although alternans of action potential and intracellularCa(2+) transients in atrial cardiomyocytesin AF have been elucidated, little is known about the mechanicalalternans, cyclic alternations in contraction force, and cardiomyocyte shortening.Moreover, the susceptibility of different regions of atria to alternansformation is unclear. The aim of this study is to analyze and comparethe parameters of alternans in sarcomere shortening-relengtheningin single cardiomyocytes isolated from the left and right atria(LA, RA) of rats with acetylcholine-CaCl2 inducedAF. We found that autonomic AF provoked mechanical alternans insingle LA and RA cardiomyocytes. We also showed that the degreeand magnitude of mechanical alternans were greater in LA cardiomyocytesthan in RA cardiomyocytes. Our results propose that LA cardiomyocyteshave a greater susceptibility to AF-induced beat-to-beat alternans insarcomere shortening amplitudes than RA myocytes that may causeLA mechanical dysfunction.

AB - Atrial fibrillation (AF) is the most common cardiac arrhythmiaaccounting for significant morbidity and mortality. Cardiac alternans,defined at the cellular level as cyclic beat-to-beat alternationsin cell contraction, action potential morphology, and intracellularCa(2+) concentration, have been associatedwith sustained AF. Although alternans of action potential and intracellularCa(2+) transients in atrial cardiomyocytesin AF have been elucidated, little is known about the mechanicalalternans, cyclic alternations in contraction force, and cardiomyocyte shortening.Moreover, the susceptibility of different regions of atria to alternansformation is unclear. The aim of this study is to analyze and comparethe parameters of alternans in sarcomere shortening-relengtheningin single cardiomyocytes isolated from the left and right atria(LA, RA) of rats with acetylcholine-CaCl2 inducedAF. We found that autonomic AF provoked mechanical alternans insingle LA and RA cardiomyocytes. We also showed that the degreeand magnitude of mechanical alternans were greater in LA cardiomyocytesthan in RA cardiomyocytes. Our results propose that LA cardiomyocyteshave a greater susceptibility to AF-induced beat-to-beat alternans insarcomere shortening amplitudes than RA myocytes that may causeLA mechanical dysfunction.

UR - https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=tsmetrics&SrcApp=tsm_test&DestApp=WOS_CPL&DestLinkType=FullRecord&KeyUT=000935467900002

U2 - 10.1134/S002209302207002X

DO - 10.1134/S002209302207002X

M3 - Article

VL - 58

SP - S13-S21

JO - Journal of Evolutionary Biochemistry and Physiology

JF - Journal of Evolutionary Biochemistry and Physiology

SN - 0022-0930

IS - S1

ER -

ID: 35452601