Effects of Acetylcholine on Electrical Remodeling of Human Atrial Fibers
Autonomic nervous system activation can result in significant changes of atrial electrophysiology and facilitate induction of atrial fibrillation. By recording influence of different concentrations of acetylcholine (ACh) on atrial fibers (AF), we investigated the role of the increased vagal tone in...
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Published in | Journal of Huazhong University of Science and Technology. Medical sciences Vol. 31; no. 2; pp. 164 - 168 |
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Main Author | |
Format | Journal Article |
Language | English |
Published |
Heidelberg
Huazhong University of Science and Technology
01.04.2011
Department of Cardiovascular Surgery%Ion Channelopathy Research Center, Institute of Cardiology, Union Hospital Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China%Department of Biological Engineering, South-Central University for Nationalities, Wuhan 430074, China |
Subjects | |
Online Access | Get full text |
ISSN | 1672-0733 1993-1352 |
DOI | 10.1007/s11596-011-0244-3 |
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Summary: | Autonomic nervous system activation can result in significant changes of atrial electrophysiology and facilitate induction of atrial fibrillation. By recording influence of different concentrations of acetylcholine (ACh) on atrial fibers (AF), we investigated the role of the increased vagal tone in electrical remodeling in atrial fibrillation. Parameters of action potentials and force contraction (Fc) in atrial fibers were recorded by using standard intracellular microelectrode technique and force transducer. It was found that: (1) ACh at 0.1 μmol/L had no significant influence on spontaneous action potentials (SAPs) and Fc (n=6, P0.05); ACh at both 1.0 and 10.0 μmol/L shortened action potential duration (APD) and Fc of human AF from right atrium (n=6, P0.05); there was no significant difference in shortening APD between 10.0 and 1.0 μmol/L of ACh; (2) ACh at 0.1 μmol/L had no significant desensitization (n=6, P0.05), but ACh at 1.0 and 10.0 μmol/L had desensitization (n=6, P0.05) to SAPs and Fc. The desensitization of ACh on APD in AF was concentration- and time-dependent. It was shown that APD was longer than the control along with extending time of continuous Tyrode's solution perfusion after desensitization. It is concluded that ACh changes the electrophysiological characteristics of human AF, indicating that increased vagal tone plays a role in the development of a vulnerable substrate for atrial electrical remodeling in atrial fibrillation. |
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Bibliography: | electrical remodeling; vagal nervous system; acetylcholine; desensitization 42-1679/R Autonomic nervous system activation can result in significant changes of atrial electrophysiology and facilitate induction of atrial fibrillation. By recording influence of different concentrations of acetylcholine (ACh) on atrial fibers (AF), we investigated the role of the increased vagal tone in electrical remodeling in atrial fibrillation. Parameters of action potentials and force contraction (Fc) in atrial fibers were recorded by using standard intracellular microelectrode technique and force transducer. It was found that: (1) ACh at 0.1 μmol/L had no significant influence on spontaneous action potentials (SAPs) and Fc (n=6, P0.05); ACh at both 1.0 and 10.0 μmol/L shortened action potential duration (APD) and Fc of human AF from right atrium (n=6, P0.05); there was no significant difference in shortening APD between 10.0 and 1.0 μmol/L of ACh; (2) ACh at 0.1 μmol/L had no significant desensitization (n=6, P0.05), but ACh at 1.0 and 10.0 μmol/L had desensitization (n=6, P0.05) to SAPs and Fc. The desensitization of ACh on APD in AF was concentration- and time-dependent. It was shown that APD was longer than the control along with extending time of continuous Tyrode's solution perfusion after desensitization. It is concluded that ACh changes the electrophysiological characteristics of human AF, indicating that increased vagal tone plays a role in the development of a vulnerable substrate for atrial electrical remodeling in atrial fibrillation. Chengkun XIA1, Jiahong XIA1#, Zhigang SHUI1, Jinping LIU1, Wei SUN1, Yimei DU2, Guoliang HAO3 1Department of Cardiovascular Surgery, 2Ion Channelopathy Research Center, Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China 3Department of Biological Engineering, South-Central University for Nationalities, Wuhan 430074, China ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1672-0733 1993-1352 |
DOI: | 10.1007/s11596-011-0244-3 |