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目的:研究肿瘤坏死因子-α(TNF-α)对体外大鼠心脏致室性心律失常的作用,初步探讨致室性心律失常的机制。方法:采用大鼠体外心脏灌流模型观察TNF-α对心脏室性心律失常的作用,通过激光共聚焦技术观察TNF-α对单个分离心肌细胞钙浓度的影响。结果:不同浓度的TNF-α灌流能引起体外心脏室性心律失常,且室性心律失常发生次数随着TNF-α浓度的增加而增多(P<0.05);经TNF-α受体抗体预处理后同等浓度的TNF-α引起的室性心律失常较前明显减少(P<0.05)。200kU/LTNF-α可使心肌胞内钙荧光强度增加(121.0±13.3)%;TNF-α受体抗体预处理,TNF-α仅能使胞内钙荧光强度增加[(13.5±3.7)%,P<0.01]。结论:TNF-α能够引起体外心脏室性心律失常,可能与TNF-α使心肌胞内钙短时间大量增加有关。
Objective: To investigate the effect of tumor necrosis factor-α (TNF-α) on ventricular arrhythmia induced by in vitro rat ventricular arrhythmia and to explore the underlying mechanism of ventricular arrhythmia. Methods: The effects of TNF-α on ventricular arrhythmias were observed by in vitro cardioplegia model in rats. The effect of TNF-α on the calcium concentration of single isolated cardiomyocytes was observed by laser scanning confocal microscope. Results: Perfusion with different concentration of TNF-α could induce ventricular arrhythmia in vitro and the number of ventricular arrhythmia increased with the increase of TNF-α concentration (P <0.05). Pretreatment with TNF-α receptor After the same concentration of TNF-α induced ventricular arrhythmia was significantly reduced (P <0.05). The intracellular calcium fluorescence intensity increased by (121.0 ± 13.3)% with 200 kU / LTNF-α, while the TNF-α increased the intracellular calcium fluorescence by 13.5 ± 3.7% P <0.01]. CONCLUSION: TNF-α can cause ventricular arrhythmia in vitro, which may be related to the massive increase of intracellular calcium in myocardial cells with TNF-α.