CAJ | 학술논문

目的比较风湿性心脏瓣膜病心房颤动患者和窦性心律患者右心房单个心肌细胞超极化激活电流(If)密度及超极化激活的环核苷酸门控(HCN)通道表达的变化.方法应用全细胞膜片钳技术记录25例房颤患者和16例窦性心律患者右心耳单个心房肌细胞If的变化,并用Westernblot法检测两组患者右心耳组织HCN通道的表达水平.结果相同激活电位时,房颤组患者右心耳单个心房肌细胞If电流密度明显大于窦性心律组,且随电位增加激活更快,尤其在-70 mV时,房颤组和窦性心律组If电流密度分别为(-43.74±2.87)和(-26.81 ±1.41)pA/pF,此时两组比较差异有统计学意义(P＜0.01).房颤组HCN2、HCN4通道表达水平分别为0.44±0.20和0.53±0.20,与窦性心律组的0.23±0.13和0.36 ±0.18比较均明显增高(P＜0.01).结论心房组织If电流密度增大及HCN通道表达上调参与了心房电重构,在房颤发生和维持中发挥作用.
목적 비교풍습성심장판막병심방전동환자화두성심률환자우심방단개심기세포초겁화격활전류(If)밀도급초겁화격활적배핵감산문공(HCN)통도표체적변화.방법 응용전세포막편겸기술기록25례방전환자화16례두성심률환자우심이단개심방기세포If적변화,병용Westernblot법검측량조환자우심이조직HCN통도적표체수평.결과 상동격활전위시,방전조환자우심이단개심방기세포If전류밀도명현대우두성심률조,차수전위증가격활경쾌,우기재-70 mV시,방전조화두성심률조If전류밀도분별위(-43.74±2.87)화(-26.81 ±1.41)pA/pF,차시량조비교차이유통계학의의(P＜0.01).방전조HCN2、HCN4통도표체수평분별위0.44±0.20화0.53±0.20,여두성심률조적0.23±0.13화0.36 ±0.18비교균명현증고(P＜0.01).결론 심방조직If전류밀도증대급HCN통도표체상조삼여료심방전중구,재방전발생화유지중발휘작용.
Objective To study the changes of both funny current (If) density and expression levels of hyperpolarization-activated cyclic nucleotide-gated (HCN) channel in muscles of right atrium in rheumatic heart disease patients with atrial fibrillation (AF) in comparison to those in normal sinus rhythm (SR).Methods Ifdensity was measured by using whole-cell patch clamp technique in single myocyte isolated by an enzymatic dissociation method from right atrial appendages in patients with AF (n =25) and those with SR (n =16).The expression levels of HCN channe1 were also determined in right atrial appendages from patients with AF and those with SR by Western boltting.Results Ifdensity in single myocyte was significantly increased at same test potential in AF compared to that in SR.And the difference reached peak with the test potential of-70 mV [(-43.74 ±2.87) vs.(-26.81 ± 1.41) pA/pF,P ＜0.01].The expression levels of HCN2 and HCN4 channels were also significantly higher in AF than those of SR [(0.44 ±0.20) vs.(0.23 ±0.13) and (0.53 ±0.20) vs.(0.36 ±0.18),P ＜0.01].Conclusion The data suggest that the increase of If density and HCN channel up-regulation might contribute to the atrial electrical remodeling which participates in the progress of AF development in rheumatic heart disease.