| Objective： To study TNF-α expression in cardiomyocytes of rats after myocardialinfarction 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) ofcoronary artery of rats we established the rat myocardial infarction model. Then weobserved whether ventricular arrhythmia could be induced by programmed electricalstimulation1day,3days,7days,14days,1month and2months after MI. The expressionof TNF-α was also examined by western blot and laser scanning confocal at the same timepoint.Results：Compared with control group, the incidence rate of induced ventricular arrhythmiaby program electric increased significantly (P <0.05) at each time point in MI group. Theexpression of TNF-α increased gradually after myocardial infarction, reaching the peak in14days after MI, then the expression reduced gradually. Compared with MI group, theincidence rate of induced ventricular arrhythmia by program electric was decreasedsignificantly (P <0.05) in rhTNFR:Fc group at each time point,, The result of Western Blotshowed TNF-α expression reduced significantly (P <0.05) as well. Conclusion：The expression of TNF-α increased significantly after myocardial infarction.The incidence rate of induced ventricular arrhythmia by program electric increasedsignificantly. Lowering the expression of TNF-α could reduce induced ventriculararrhythmia. TNF-α may play an important role in the occurrence of ventricular arrhythmiaafter myocardial infarction. Objective：To study Cx43expression in cardiomyocytes of rats after myocardial infarctionand its role on ventricular arrhythmias after myocardial infarction.Methods：240male SD rats were randomly divided into control group and myocardialinfarction group. By ligation the left anterior descending (LAD) of coronary artery of ratswe established the rat myocardial infarction model. Then we observed whether ventriculararrhythmia could be induced by programmed electrical stimulation1day,3days,7days,14days,1month and2months after MI. The expression of Cx43was also examined bywestern blot and laser scanning confocal at the same time point.Results：Compared with control group, the incidence rate of induced ventricular arrhythmiaby program electric increased significantly (P <0.05) at each time point in MI group. Theexpression of nonphoshporylated Cx43increased and the expression of phoshporylatedCx43decreased after myocardial infarction. The abnormal expression and distribution ofCx43changed 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 arrhythmiaafter myocardial infarction. Objective: To study the relationship of TNF-α on regulation of Cx43and ventriculararrhythmias 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) ofcoronary artery of rats we established the rat myocardial infarction model. Then weobserved whether ventricular arrhythmia could be induced by programmed electricalstimulation1day,3days,7days,14days,1month and2months after MI. The expressionof TNF-α and Cx43was also examined by western blot and laser scanning confocal at thesame time point.Results：Compared with control group, the incidence rate of induced ventricular arrhythmiaby program electric increased significantly (P <0.05) at each time point in MI group. Theexpression of TNF-α increased gradually after myocardial infarction; The expression ofnonphoshporylated Cx43increased and the expression of phoshporylated Cx43decreasedafter myocardial infarction. These change reached the peak in14days after MI, and theabnormal was stable from then on. Compared with MI group, the incidence rate of inducedventricular arrhythmia by program electric was increased significantly (P <0.05) inrhTNFR:Fc group at each time point. The result of Western Blot showed TNF-α expressionreduced significantly (P <0.05) as well.Conclusion: The high expression of TNF-α can induce the nonphosphorylated refactoringand abnormal distribution of Cx43, thus play an important role in the occurrence ofventricular arrhythmia after myocardial infarction. |
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