Background:The adipocytokine resistin is released from epicardial adipose tissue (EAT). Plasma resistin and EAT deposition are independently associated with atrial fibrillation (AF). The EAT secretome enhances arrhythmia susceptibility and inotropy of human myocardium. Therefore, we aimed to determine the effect of resistin on the function of human myocardium and how resistin contributes to the pro-arrhythmic effect of EAT. Methods & Results: EAT biopsies were obtained from 25 cardiac surgery patients. Resistin levels were measured by ELISA in 24-hour EAT culture media (n=8). The secretome resistin concentrations increased over the culture period to a maximal level of 5.9 ± 1.2 ng/mL. Co-culture with β-adrenergic agonists isoproterenol (n=4) and BRL37344 (n=13) had no effect on EAT resistin release. Addition of resistin (7, 12, 20 ng/mL) did not significantly increase the spontaneous contraction propensity of human atrial trabeculae (n=10) when given alone or in combination with isoproterenol. Resistin dose-dependently increased trabecula developed force (maximal 2.9-fold increase, P< 0.0001), as well as the maximal rates of contraction (2.6-fold increase, P= 0.002) and relaxation (1.8-fold increase,P= 0.007). Additionally, the post-rest potentiation capacity of human trabeculae was reduced at all resistin doses, suggesting that the inotropic effect induced by resistin might be due to altered sarcoplasmic reticulum Ca²⁺-handling. Conclusions: EAT resistin release is not modulated by common arrhythmia triggers. Furthermore, exogenous resistin does not promote arrhythmic behaviour in human atrial trabeculae. Resistin does, however, induce an acute dose-dependent positive inotropic and lusitropic effect.

中文翻译：

---

促肌力和促尿嘧啶，但不致心律失常，对人心房心肌的作用。

背景：脂肪细胞因子抵抗素从心外膜脂肪组织（EAT）中释放。血浆抵抗素和EAT沉积与房颤（AF）独立相关。EAT分泌组可增强人心肌的心律失常敏感性和正性肌力。因此，我们旨在确定抵抗素对人心肌功能的影响以及抵抗素如何促进EAT的心律失常作用。方法与结果：从25例心脏外科手术患者中获得EAT活检。通过ELISA在24小时EAT培养基（n = 8）中测量抵抗素水平。在培养期间，分泌素抵抗素浓度增加至最大水平5.9±1.2 ng / mL。与β-肾上腺素能激动剂异丙肾上腺素（n = 4）和BRL37344（n = 13）共培养对EAT抵抗素释放没有影响。添加抵抗素（7，12，当单独或与异丙肾上腺素联合使用时，20 ng / mL）不会显着增加人房小梁的自发收缩倾向（n = 10）。抵抗素剂量依赖性地增加小梁发展力（最大增加2.9倍，P <0.0001），以及最大收缩率（增加2.6倍，P = 0.002）和松弛率（增加1.8倍，P = 0.007） 。此外，在所有抵抗素剂量下，人小梁的休息后增强能力都会降低，这表明抵抗素诱导的肌力作用可能是由于肌浆网钙的改变 0001），以及最大收缩率（增加2.6倍，P = 0.002）和放松（增加1.8倍，P = 0.007）。此外，在所有抵抗素剂量下，人小梁的休息后增强能力都会降低，这表明抵抗素诱导的肌力作用可能是由于肌浆网钙的改变 0001），以及最大收缩率（增加2.6倍，P = 0.002）和放松（增加1.8倍，P = 0.007）。此外，在所有抵抗素剂量下，人小梁的休息后增强能力都会降低，这表明抵抗素诱导的肌力作用可能是由于肌浆网钙的改变^2+处理。结论：EAT抵抗素释放不受常见的心律不齐触发器的调节。此外，外源抵抗素不会促进人房小梁的心律失常行为。然而，抵抗素确实会引起急性的剂量依赖性正性肌力和促肌力作用。