Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3447075 | Archives of Medical Research | 2008 | 7 Pages |
BackgroundTumor necrosis factor-α (TNF-α) is found to play important roles in acute myocardial infarction (AMI). Ventricular arrhythmias arising from AMI are leading causes of sudden cardiac death (SCD). We sought to clarify the effect of TNF-α early expression on ventricular arrhythmias in rats with AMI and its mechanism.MethodsRats with AMI were induced by left anterior descending coronary branch ligation. The mRNA and protein levels of TNF-α in myocardium were detected by real-time fluorescent quantitative PCR, Western blotting and histochemistry. Meanwhile, electrocardiogram was recorded. Different concentrations of TNF-α were added to isolated rat hearts in isolated heart perfusions. Effect of TNF-α on intracellular Ca2+ concentration was detected by laser confocal technique.ResultsIn AMI rats, mRNA and protein levels of TNF-α were higher than control (p <0.05), and the occurrence time of ventricular arrhythmias coincided with the secretion of TNF-α. TNF-α may cause ventricular arrhythmias in isolated rat heart perfusion models. Intracellular Ca2+ intensity may quickly be increased by TNF-α.ConclusionsOur results reveal the positive correlation between TNF-α early expression and ventricular arrhythmias in rats with AMI. This effect may be associated with the increased intracellular Ca2+ intensity caused by TNF-α.