Effect of Tumor Necrosis Factor-α on Neutralization of Ventricular Fibrillation in Rats with Acute Myocardial Infarction

Abstract

The purpose of this study was to explore the effects of tumor necrosis factor-α (TNF-α) on ventricular fibrillation (VF) in rats with acute myocardial infarction (AMI). Rats were randomly classified into AMI group, sham operation group and recombinant human tumor necrosis factor receptor:Fc fusion protein (rhTNFR:Fc) group. Spontaneous and induced VFs were recorded. Monophasic action potentials (MAPs) among different zones of myocardium were recorded at eight time points before and after ligation and MAP duration dispersions (MAPDds) were calculated. Then expression of TNF-α among different myocardial zones was detected. After ligation of the left anterior descending coronary artery, total TNF-α expression in AMI group began to markedly increase at 10 min, reached a climax at 20–30min, and then gradually decreased. The time-windows of VFs and MAPDds in the border zone performed in a similar way. At the same time-point, the expression of TNF-α in the ischemia zone was greater than that in the border zone, and little in the non-ischemia zone. Although the time windows of TNF-α expression, the MAPDds in the border zone and the occurrence of VFs in the rhTNFR:Fc group were similar to those in the AMI group, they all decreased in the rhTNFR:Fc group. Our findings demonstrate that TNF-α could enlarge the MAPDds in the border zone, and promote the onset of VFs.

Decreased prevalence of cardiac arrhythmias during and after vigorous and prolonged exercise in healthy male marathon runners

“…31 Associations to atrial and ventricular arrhythmias have also been described. [32][33][34] However, in our cohort, exercise-induced increases of neither IL-6 nor hs-cTNT were associated with changes of premature beats in Holter ECG during marathon. IN addition, electrolytes were in the reference range in our cohort.…”

Atorvastatin administered before myocardial infarction in rats improves contractility irrespective of metabolic changes

“…Increased expression of pro‐inflammatory cytokines (tumor necrosis factor‐α (TNF‐α) and interleukin (IL‐6) occurs in the heart after an acute myocardial infarction . By contrast, IL‐10 is considered a major anti‐inflammatory cytokine and, as a compensatory mechanism, it might acutely increase after cardiac injury .…”

Effect of lysophosphatidic acid on the immune inflammatory response and the connexin 43 protein in myocardial infarction

“…TNF-α is a multifunctional cytokine; as a key inflammatory mediator of AMI, TNF-α has been the subject of increased research. Animals overexpressing TNF suffer from severe heart disease, including arrhythmia (26)(27)(28). This indicates that upregulation of TNF expression is closely associated with the dysfunction of cardiac myocytes (29,30).…”