Effects of tumor necrosis factor-α on ventricular arrhythmias in rats with acute myocardial infarction
10.3760/cma.j.issn.1671-0282.2010.07.010
- VernacularTitle:急性心肌梗死大鼠肿瘤坏死因子α表达与室性心律失常的关系
- Author:
Yu CHEN
;
Zhijian CHEN
;
Yuhua LIAO
;
Zhe CAO
;
Jiading XIA
;
Hua YANG
;
Yimei DU
- Publication Type:Journal Article
- Keywords:
Acute myocardial infarction;
Tumor necrosis factor-α;
Ventricular arrhythmia;
Recombinant human tumor necrosis factor receptor:Fc fusion protein(rhTNFR: Fc)
- From:
Chinese Journal of Emergency Medicine
2010;19(7):712-716
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effects of tumor necrosis factor-α (TNF-α) on ventricular arrhythmias resulted from acute myocardial infarction (AMI) in rats. Method Two hundred and forty male Wistar rats were randomized (random number) into sham operation group, AMI group and recombinant human tumor necrosis factor receptor (rhTNFR) fusion protein (Fc) group. Acute anterior wall myocardial infarction was produced in rats of AMI group with ligating the left anterior descending coronary artery (LAD) , and the rats were just operated without ligation of LAD in sham group. The rats of Fc group were treated with rhTNFR-Fc (10 mg/kg), a TNF-α antagonist, 24 hours before LAD ligation. The original ECG was recorded 10 min before ligation and the ECGs of ventricular arrhythmias occurred spontaneously or induced by programmed electrical stimulation were recorded 10 min, 20 min, 30 min, 60 min, 3 h, 6 h and 12 hours after ligation. The protein levels and mRNA expressions of TNF-α in rats in different groups were detected with histochemistry and real-time fluorescent quantitative PCR. Results The expressions of TNF-α mRNA and levels of TNF-α protein markedly increased 10 min after infarction, reached the climax 20-30 min later, and then gradually returned to the original level in AMI group and Fc group. The time-windows of spontaneous and induced ventricular arrhythmias were consistent with the time-window of expressions of TNF-α mRNA and levels of TNF-α protein. Compared with AMI group, there were lower levels of TNF-α protein and lower incidence of ventricular arrhythmias in Fc group ( P < 0.05) , but there was no significant difference in TNF-α mRNA between two groups. There was no obvious change in TNF-α in rats of sham operation group. Conclusions The expressions of TNF-α mRNA and levels of TNF-α protein induced by AMI could contribute the initiation of ventricular arrhythmias.
