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目的 研究风湿性心脏病 (RHD)慢性心房颤动 (房颤 )使心房肌细胞膜超快速激活钾电流 (IKur)的变化 ,探讨离子通道改变在房颤时心房电重构 (AER)中的作用。方法 采集 2 3例RHD患者(房颤组 12例 ,窦性心律组 11例 )心房肌标本 ,采用急性酶解法 ,将组织块分解以获得游离的心房肌细胞 ;应用膜片钳全细胞技术 ,记录两组患者心房肌细胞膜IKur电流 ,并对比分析两组的电流 电压曲线以及稳态激活和失活的动力学特性。结果 在钳制电位 + 10mV～ + 50mV时 ,房颤组IKur密度明显低于窦性心律组 (P <0 0 5) ;其中 ,除极化至 + 50mV时 ,密度分别为 (4 92± 1 48)pA/pF(n =19个细胞 )和 (9 3 1± 1 44) pA /pF(n =2 1个细胞 ,P <0 0 1)。房颤组右心房细胞IKur的激活最大电导较窦性心律组明显降低 ,分别为 (2 75± 0 55)nS(n =2 1个细胞 )和 (4 74± 0 63 )nS(n =2 1个细胞 ,P <0 0 1)。房颤组在 + 50mV时的失活率为 56% ,低于窦性心律组 (P <0 0 5) ,而两组的稳态激活和失活特征的差异无显著性。结论 现有数据显示 ,IKur密度的改变可能是慢性房颤时AER中多种离子通道重构的重要机制之一 ,可能与房颤时心肌细胞的传导性、不应期等改变有关 ,与房颤发生和持续的关系和潜在的治疗性意义尚需进一步研究阐明
Objective To study the changes of IKUR in atrial fibrillation induced by chronic atrial fibrillation (AF) in rheumatic heart disease (RHD) and to explore the role of ion channel changes in atrial electrical remodeling (AER) during atrial fibrillation. Methods Twenty-three subjects with atrial fibrillation (12 patients with atrial fibrillation and 11 patients with sinus rhythm) were enrolled in this study. Atrial fibrillation was performed using an acute enzymolysis method to obtain free atrial myocytes. Using patch-clamp whole cell technique, The atrial muscle cell membrane IKur current was recorded in both groups, and the current and voltage curves and the dynamic characteristics of steady-state activation and inactivation were compared between the two groups. Results The density of IKur in atrial fibrillation group was significantly lower than that in sinus rhythm group (P <0.05) at the clamping potential of +10 mV to +50 mV; the densities were (4 92 ± 1 48) ) pA / pF (n = 19 cells) and (931 ± 1 44) pA / pF (n = 21 cells, P <0.01). The maximal conductance of IKur in atrial fibrillation group was significantly lower than that in sinus rhythm group (n = 2 75 ± 0 55) and 4 74 ± 0 63 nS (n = 2 1 cell, P <0.01). In AF group, the inactivation rate at +50 mV was 56%, which was lower than that in sinus rhythm group (P <0.05). There was no significant difference between the two groups in the steady-state activation and inactivation characteristics. Conclusions The available data show that the change of IKur density may be one of the important mechanisms of the remodeling of many ion channels in AER during chronic atrial fibrillation, which may be related to the changes of cardiomyocyte conductivity, refractory period and so on during atrial fibrillation. The occurrence and persistence of fibrillation and the potential therapeutic significance need further elucidation