心房有效不应期（AERP）缩短是心房颤动（AF）发病的关键环节，延长AERP是治疗AF的重要手段。研究发现心肌细胞骨架蛋白Yotiao可增强缓慢激活延迟整流钾通道（Iks）电流，而Iks电流是AERP重要组成部分，这提示抑制Yotiao的基因表达将减少Iks电流，延长AERP，为AF治疗提供可能途径，但是此假设尚需验证。本研究拟在我们前期建立心肌细胞快速起搏模型与兔AF模型的基础上，利用RNA干扰，用短发夹RNA（shRNA）分别感染心房肌细胞快速起搏模型和兔AF模型，检测Iks、AERP、Yotiao量的变化及其对AF的影响，在细胞和整体水平验证假设，探索AF治疗的新方法。

A shortened atrial effective refractory period(AERP) is the original pathological factor in atrial fibrillation(AF). Thus prolonging AERP could bring a potential way for AF treatment. AERP is mainly determined by the slow-delayed rectifier K+ channel current(Iks).Some studies found that Yotiao,a myocardial skeleton protein,was closely related to the enhancement of Iks. In our previous study we established the rapid pacing atrial cell model and animal AF model. We thus hypothesize that inhibiting Yotiao's expression could reduce Iks current from the origin and prolong AERP. In this study, in order to explore effective way for AF treatment, we plan to down-regulate the expression of Yotiao and to prolong AERP by transfecting a viral vector containing short hairpin RNA（shRNA) into rapid pacing single cell model as well as into left atrium and pulmonary vein antrium in rabbit AF model.