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Role of Tumor Necrosis Factor-α in the Pathogenesis of Atrial Fibrosis and Development of an Arrhythmogenic Substrate

机译:肿瘤坏死因子-α在心房纤维化的发病机理和心律失常基质的发展中的作用

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Background: ?Although tumor necrosis factor-α (TNF-α) levels are increased in patients with atrial fibrillation (AF), its role in the pathogenesis of AF is unclear. We investigated whether direct delivery of TNF-α could induce atrial fibrosis. Methods and Results: ?TNF-α (4μg/kg) was injected into the tail vein of 20 male Swiss albino mice (TNF group) and saline into 20 control mice (CON group). The dose was carefully chosen to avoid any significant decrease in left ventricular (LV) function. Animals were killed after 16 weeks and their atria examined for fibrosis. We found increased atrial fibrosis in the TNF group compared with the CON group [372.8±21.5 arbitrary units (a.u.) vs. 56.9±6.5 a.u., respectively, mean±SEM; P
机译:背景:尽管房颤(AF)患者的肿瘤坏死因子-α(TNF-α)水平升高,但其在AF发病机理中的作用尚不清楚。我们调查了TNF-α的直接递送是否可以诱导心房纤维化。方法与结果:将TNF-α(4μg/ kg)注射入20只瑞士白化病雄性小鼠(TNF组)的尾静脉中,并将生理盐水注射入20只对照小鼠(CON组)中。谨慎选择剂量以避免左心室(LV)功能显着降低。 16周后处死动物,检查其心房纤维化。与CON组相比,我们发现TNF组的房纤维化增加[分别为372.8±21.5个任意单位(a.u.)和56.9±6.5 a.u.,均值±SEM]。 P

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