Slow conduction and gap junction remodeling in murine ventricle after chronic alcohol ingestion

Journal of Biomedical Science

Research

Ya-Ming Tseng¹  Yu-Jun Lai¹  Hung-I Yeh¹  Cheng-Ho Tsai¹  Chung-Lieh Hung¹  Ray-Ching Hong¹  Cheng-I Lin²  Yu-Shien Ko³ 

[1] Departments of Internal Medicine and Medical Research, Mackay Memorial Hospital, Mackay Medicine, Nursing and Management College, Mackay Medical College, New Taipei City, Taiwan;Departments of Physiology and Biophysics, National Defense Medical Center, Taipei, Taiwan;The First Cardiovascular Division, Department of Internal Medicine, Chang Gung Memorial Hospital, Taipei, Taiwan;

关键词: alcohol;    arrhythmia;    remodeling;    gap junctions;    optical mapping;   

DOI  :  10.1186/1423-0127-18-72

 received in 2011-07-11, accepted in 2011-09-29,  发布年份 2011

来源: Springer

【 摘 要 】

BackgroundLong-term heavy alcohol drinkers are prone to the development of cardiac arrhythmia. To understand the mechanisms, we evaluated the cardiac structural and electrophysiological changes in mice chronically drinking excessive alcohol.ResultsMale C57BL/6J mice were given 36% alcohol in the drinking water. Those given blank water were used as control. Twelve weeks later, the phenotypic characteristics of the heart, including gap junctions and electrical properties were examined. In the alcohol group the ventricles contained a smaller size of cardiomyocytes and a higher density of capillary networks, compared to the control. Western blots showed that, after drinking alcohol, the content of connexin43 (Cx43) protein in the left ventricle was increased by 18% (p < 0.05). Consistently, immunoconfocal microscopy demonstrated that Cx43 gap junctions were up-regulated in the alcohol group with a disorganized distribution, compared to the control. Optical mapping showed that the alcohol group had a reduced conduction velocity (40 ± 18 vs 60 ± 7 cm/sec, p < 0.05) and a higher incidence of ventricular tachyarrhythmia (62% vs 30%, p < 0.05).ConclusionLong-term excessive alcohol intake resulted in extensive cardiac remodeling, including changes in expression and distribution of gap junctions, growth of capillary network, reduction of cardiomyocyte size, and decrease of myocardial conduction.

【 授权许可】

Unknown   
© Lai et al; licensee BioMed Central Ltd. 2011. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.