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目的比较持续性心房颤动患者(房颤组)和正常窦性心律患者(窦律组)右心耳单个心房肌细胞内向整流钾通道电流(IK1)密度的变化及其亚基Kir2．1mRNA表达的变化。方法用常规全细胞膜片钳技术记录了8例风湿性心脏病房颤患者和12例窦律患者急性酶分离法分离的右心耳单个心房肌细胞,IK1的变化；用半定量一步法RT—PCR技术检测了19例房颤患者和18例窦律患者右心耳组织内向整流钾通道亚基Kir2．1mRNA的表达。结果房颤组患者右心耳单个心房肌细胞IK1电流密度在电位水平更负时比窦律组明显升高,且电流升高只发生在静息电位水平更负的细胞,平均静息膜电位分别为(-78．95±4．67)mV和(-70．22±11．08)mV,P>0．05；超级化至-100mV时IK1电流密度分别为(-9．59±2．47)pA／pF(n=15个细胞)和(-5．58±2．52)pA／pF(n=26个细胞),P<0．01。Kir2．1mRNA水平与对照组相比,升高了47．81％,为0．50±0．16与0．34±0．09,P<0．05。结论Kir2．1mRNA表达升高可能是IK1电流升高的分子基础,IK1电流升高及其基因表达上调是房颤离子重构的机制之一,在房颤电重构中发挥一定的作用。
Objective To compare the changes of inward rectifier potassium channel current (IK1) density and Kir2.1 mRNA expression in atrial myocytes of patients with persistent atrial fibrillation (AF) and normal sinus rhythm (sinus rhythm group) . Methods The changes of IK1 in single atrial myocytes of right atrial appendage isolated from acute rheumatic heart disease in 8 patients with rheumatic heart disease and 12 patients with sinus rhythm were recorded by conventional whole-cell patch clamp technique. Semi-quantitative one-step RT-PCR Technology was used to detect Kir2.1 mRNA expression in the inward rectifier potassium channel subunit of right atrial appendage in 19 patients with AF and 18 patients with sinus rhythm. Results The current density of IK1 in atrial myocytes in atrial fibrillation group was significantly higher than that in sinus rhythm group when the potential level was more negative, and the current rise occurred only in cells with more negative resting potential. The average resting membrane potential (-78.95 ± 4.67) mV and (-70.22 ± 11.08) mV, P> 0.05 respectively. The current density of IK1 at hypermytosis to -100mV was (-9.59 ± 2) 47) pA / pF (n = 15 cells) and (-5.58 ± 2.52) pA / pF (n = 26 cells), P <0.01. Compared with the control group, Kir2.1 mRNA level increased by 47.81%, which was 0.50 ± 0.16 and 0.34 ± 0.09, P <0.05. Conclusions Elevated Kir2.1 mRNA expression may be the molecular basis of IK1 current. Upregulation of IK1 current and up-regulation of IK1 gene may play an important role in the remodeling of atrial fibrillation.