Positive correlation of tumor necrosis factor-α early expression in myocardium and ventricular arrhythmias in rats with acute myocardial infarction

被引:27
作者
Xiao, Hua [1 ]
Chen, Zhijian [1 ]
Liao, Yuhua [1 ]
Cheng, Xiang [1 ]
Liu, Kun [1 ]
Wang, Yanfu [1 ]
Wang, Min [1 ]
Guo, Heping [1 ]
机构
[1] Hua Zhong Univ Sci & Technol, Lab Cardiovasc Immunol, Union Hosp,Inst Cardiol, Tong Ji Med Coll, Wuhan 430022, Hubei Province, Peoples R China
关键词
myocardial infarction; tumor necrosis factor-alpha; arrhythmia; calcium channels; sudden cardiac death;
D O I
10.1016/j.arcmed.2007.10.004
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Background. Tumor necrosis factor-alpha (TNF-alpha) is found to play important roles in acute myocardial infarction (AMI). Ventricular arrhythmias arising from AMI are le ading causes of sudden cardiac death (SCD). We sought to clarify the effect of TNF-alpha early expression on ventricular arrhythmias in rats with AMI and its mechanism. Methods. Rats with AMI were induced by left anterior descending coronary branch ligation. The mRNA and protein levels of TNF-alpha in myocardium were detected by real-time fluorescent quantitative PCR, Western blotting and histochemistry. Meanwhile, electrocardiogram was recorded. Different concentrations of TNF-alpha were added to isolated rat hearts in isolated heart perfusions. Effect of TNF-alpha on intracellular Ca2+ concentration was detected by laser confocal technique. Results. In AMI rats, mRNA and protein levels of TNF-alpha were higher than control (p < 0.05), and the occurrence time of ventricular arrhythmias coincided with the secretion of TNF-alpha. TNF-alpha may cause ventricular arrhythmias in isolated rat heart perfusion models. Intracellular Ca2+ intensity may quickly be increased by TNF-alpha. Conclusions. Our results reveal the positive correlation between TNF-alpha early expression and ventricular arrhythmias in rats with AMI. This effect may be associated with the increased intracellular Ca2+ intensity caused by TNF-alpha. (c) 2008 IMSS. Published by Elsevier Inc.
引用
收藏
页码:285 / 291
页数:7
相关论文
共 35 条
[21]  
Myerburg RJ, 1998, CIRCULATION, V97, P1514
[22]   Endothelin A receptor blockade causes adverse left ventricular remodeling but improves pulmonary artery pressure after infarction in the rat [J].
Nguyen, QT ;
Cernacek, P ;
Calderoni, A ;
Stewart, DJ ;
Picard, P ;
Sirois, P ;
White, M ;
Rouleau, JL .
CIRCULATION, 1998, 98 (21) :2323-2330
[23]   Electrical remodeling of cardiac myocytes from mice with heart failure due to the overexpression of tumor necrosis factor-α [J].
Petkova-Kirova, PS ;
Gursoy, E ;
Mehdi, H ;
McTiernan, CF ;
London, B ;
Salama, G .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2006, 290 (05) :H2098-H2107
[24]   Atrial contractile dysfunction, fibrosis, and arrhythmias in a mouse model of cardiomyopathy secondary to cardiac-specific overexpression of tumor necrosis factor-α [J].
Saba, S ;
Janczewski, AM ;
Baker, LC ;
Shusterman, V ;
Gursoy, EC ;
Feldman, AM ;
Salama, G ;
McTiernan, CF ;
London, B .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2005, 289 (04) :H1456-H1467
[25]   C-reactive protein and atrial fibrillation - Is inflammation a consequence or a cause of atrial fibrillation? [J].
Sata, N ;
Hamada, N ;
Horinouchi, T ;
Amitani, S ;
Yamashita, T ;
Moriyama, Y ;
Miyahara, K .
JAPANESE HEART JOURNAL, 2004, 45 (03) :441-445
[26]   Tumor necrosis factor-α-converting enzyme and tumor necrosis factor-α in human dilated cardiomyopathy [J].
Satoh, M ;
Nakamura, M ;
Saitoh, H ;
Satoh, H ;
Maesawa, C ;
Segawa, N ;
Tashiro, A ;
Hiramori, K .
CIRCULATION, 1999, 99 (25) :3260-3265
[27]   Activated tumour necrosis factor-α shedding process is associated with in-hospital complication in patients with acute myocardial infarction [J].
Shimoda, Y ;
Satoh, M ;
Nakamura, M ;
Akatsu, T ;
Hiramori, K .
CLINICAL SCIENCE, 2005, 108 (04) :339-347
[28]   Bioactive peptide signaling within the myocardial interstitium and the matrix metalloproteinases [J].
Spinale, FG .
CIRCULATION RESEARCH, 2002, 91 (12) :1082-1084
[29]   Excessive tumor necrosis factor activation after infarction contributes to susceptibility of myocardial rupture and left ventricular dysfunction [J].
Sun, M ;
Dawood, F ;
Wen, WH ;
Chen, MY ;
Dixon, I ;
Kirshenbaum, LA ;
Liu, PP .
CIRCULATION, 2004, 110 (20) :3221-3228
[30]   Identification of direct genomic targets downstream of the nuclear factor-κB transcription factor mediating tumor necrosis factor signaling [J].
Tian, B ;
Nowak, DE ;
Jamaluddin, M ;
Wang, SF ;
Brasier, AR .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (17) :17435-17448