| Objective:To study TNF-a expression in cardiomyocytes of rats after myocardial infarction and its role on ventricular arrhythmias after myocardial infarction.Methods:360male SD rats were randomly divided into control group, rhTNFR:Fc group, and myocardial infarction group. By ligation the left anterior descending (LAD) of coronary artery of rats we established the rat myocardial infarction model. Then we observed whether ventricular arrhythmia could be induced by programmed electrical stimulation1day,3days,7days,14days,1month and2months after MI. The expression of TNF-a was also examined by western blot and laser scanning confocal at the same time point.Results:Compared with control group, the incidence rate of induced ventricular arrhythmia by program electric increased significantly (P<0.05) at each time point in MI group. The expression of TNF-a increased gradually after myocardial infarction, reaching the peak in14days after MI, then the expression reduced gradually. Compared with MI group, the incidence rate of induced ventricular arrhythmia by program electric was decreased significantly (P<0.05) in rhTNFR:Fc group at each time point,, The result of Western Blot showed TNF-a expression reduced significantly (P<0.05) as well. Conclusion:The expression of TNF-a increased significantly after myocardial infarction. The incidence rate of induced ventricular arrhythmia by program electric increased significantly. Lowering the expression of TNF-a could reduce induced ventricular arrhythmia. TNF-a may play an important role in the occurrence of ventricular arrhythmia after myocardial infarction. Objective:To study Cx43expression in cardiomyocytes of rats after myocardial infarction and its role on ventricular arrhythmias after myocardial infarction.Methods:240male SD rats were randomly divided into control group and myocardial infarction group. By ligation the left anterior descending (LAD) of coronary artery of rats we established the rat myocardial infarction model. Then we observed whether ventricular arrhythmia could be induced by programmed electrical stimulation1day,3days,7days,14days,1month and2months after MI. The expression of Cx43was also examined by western blot and laser scanning confocal at the same time point.Results:Compared with control group, the incidence rate of induced ventricular arrhythmia by program electric increased significantly (P<0.05) at each time point in MI group. The expression of nonphoshporylated Cx43increased and the expression of phoshporylated Cx43decreased after myocardial infarction. The abnormal expression and distribution of Cx43changed gradually after myocardial infarction, reaching the peak in14days after MI, being stable from then on.Conclusion:Cx43may play an important role in the occurrence of ventricular arrhythmia after myocardial infarction. Objective:To study the relationship of TNF-a on regulation of Cx43and ventricular arrhythmias after myocardial infarction in rats.Methods:360male SD rats were randomly divided into control group, rhTNFR:Fc group, and myocardial infarction group. By ligation the left anterior descending (LAD) of coronary artery of rats we established the rat myocardial infarction model. Then we observed whether ventricular arrhythmia could be induced by programmed electrical stimulation1day,3days,7days,14days,1month and2months after MI. The expression of TNF-a and Cx43was also examined by western blot and laser scanning confocal at the same time point.Results:Compared with control group, the incidence rate of induced ventricular arrhythmia by program electric increased significantly (P<0.05) at each time point in MI group. The expression of TNF-a increased gradually after myocardial infarction; The expression of nonphoshporylated Cx43increased and the expression of phoshporylated Cx43decreased after myocardial infarction. These change reached the peak in14days after MI, and the abnormal was stable from then on. Compared with MI group, the incidence rate of induced ventricular arrhythmia by program electric was increased significantly (P<0.05) in rhTNFR:Fc group at each time point. The result of Western Blot showed TNF-a expression reduced significantly (P<0.05) as well.Conclusion:The high expression of TNF-a can induce the nonphosphorylated refactoring and abnormal distribution of Cx43, thus play an important role in the occurrence of ventricular arrhythmia after myocardial infarction. |
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