CAJ | 학술논문

目的探讨家兔左心房后壁(LAPW)和左心耳底部组织(LAA)心肌细胞瞬时外向钾电流(I_(to))及L-型钙电流(I_(Ca-L))的特征以及哇巴因对其影响,提供LAPW和哇巴因在引起家兔左心房电不均一性和离子通道重构的电生理基础.方法使用离体心脏灌流系统灌注心脏,酶解法分离家兔LAPW和LAA心肌细胞.全细胞膜片钳技术记录两个部位心肌细胞I_(to)和I_(Ca-L)观察哇巴因作用前后I_(to)和I_(Ca-L)的变化,及其拟合后电流-电压(I-V)曲线改变.结果 (1)根据记录I_(to)电压钳制方案,当电位为+50 mV时,在正常对照组,LAPW心肌细胞I_(to)与LAA心房肌细胞I_(to)相比差异无统计学意义(P>0.05).但经哇巴因作用后,LAPW心肌细胞I_(to)的电流密度为(10.97±0.58)pA/pF(P<0.01),LAA心房肌细胞I_(to)的电流密度为(9.39±0.83)pA/pF(与正常对照组和LAPW心肌细胞I_(to)相比,P<0.05).LAPW心肌细胞I_(to)的I-V曲线在原来最底部移到最上部.所有I-V曲线方向没有发生改变.(2)在记录I_(Ca-L)钳制方式下,正常对照组的LAPW心肌细胞I_(Ca-L)的最大电流密度明显小于LAA心房肌细胞I_(Ca-L)的最大电流密度(P<0.05).但经哇巴因作用后,LAPW心肌细胞I_(Ca-L)最大电流密度为(-11.13±0.99)pA/pF,LAA心房肌细胞I_(Ca-L)为(-8.86±0.51)pA/pF(P<0.01).在正常对照组,LAPW心肌细胞I_(Ca-L)的I-V曲线位于最底部,经哇巴因作用后,LAPW心肌细胞I_(Ca-L)的I-V曲线上移到其他I-V曲线的最上部.每组I_(Ca-L)的I-V曲线整个形态没有发生明显变化,峰值的方向没有发生改变.结论 LAPW心肌细胞存在离子流特异性差异,哇巴因加重LAPW心肌细胞I_(to)和I_(Ca-L)大小异质性和重新分配,这可能成为心房颤动易发性的启动因素和维持条件.
목적 탐토가토좌심방후벽(LAPW)화좌심이저부조직(LAA)심기세포순시외향갑전류(I_(to))급L-형개전류(I_(Ca-L))적특정이급왜파인대기영향,제공LAPW화왜파인재인기가토좌심방전불균일성화리자통도중구적전생리기출.방법 사용리체심장관류계통관주심장,매해법분리가토LAPW화LAA심기세포.전세포막편겸기술기록량개부위심기세포I_(to)화I_(Ca-L)관찰왜파인작용전후I_(to)화I_(Ca-L)적변화,급기의합후전류-전압(I-V)곡선개변.결과 (1)근거기록I_(to)전압겸제방안,당전위위+50 mV시,재정상대조조,LAPW심기세포I_(to)여LAA심방기세포I_(to)상비차이무통계학의의(P>0.05).단경왜파인작용후,LAPW심기세포I_(to)적전류밀도위(10.97±0.58)pA/pF(P<0.01),LAA심방기세포I_(to)적전류밀도위(9.39±0.83)pA/pF(여정상대조조화LAPW심기세포I_(to)상비,P<0.05).LAPW심기세포I_(to)적I-V곡선재원래최저부이도최상부.소유I-V곡선방향몰유발생개변.(2)재기록I_(Ca-L)겸제방식하,정상대조조적LAPW심기세포I_(Ca-L)적최대전류밀도명현소우LAA심방기세포I_(Ca-L)적최대전류밀도(P<0.05).단경왜파인작용후,LAPW심기세포I_(Ca-L)최대전류밀도위(-11.13±0.99)pA/pF,LAA심방기세포I_(Ca-L)위(-8.86±0.51)pA/pF(P<0.01).재정상대조조,LAPW심기세포I_(Ca-L)적I-V곡선위우최저부,경왜파인작용후,LAPW심기세포I_(Ca-L)적I-V곡선상이도기타I-V곡선적최상부.매조I_(Ca-L)적I-V곡선정개형태몰유발생명현변화,봉치적방향몰유발생개변.결론 LAPW심기세포존재리자류특이성차이,왜파인가중LAPW심기세포I_(to)화I_(Ca-L)대소이질성화중신분배,저가능성위심방전동역발성적계동인소화유지조건.
Objective To investigate the properties of electrophysiology and effects of ouabain upon transient outward potassium current (I_(to)) and L-type calcium current (I_(Ca-L)) of left atrium posterior wall (LAPW) and left atrium appendage tissue (LAA)in rabbit so as to provide the scientific explanations that LAPW and ouabain can enhance atrial fibrillation (AF) vulnerability through increasing electrophysiological heterogeneity and electrical remodeling of different regions of left atrium in rabbits. Methods Atrial myocytes from LAPWs and LAAs of rabbits on an in vitro heart perfusion system were obtained by enzymatic dissociation. The whole-cell patch-clamp technique was used to assess the effects of ouabain upon I_(to) and I_(Ca-L). The current-voltage (I-V) curves of I_(to) and I_(Ca-L) in LAPW and LAA myocytes were fitted before and after ouabain administration. Results (1) With holding potential + 50 mV and commanding potential + 50 mV, the current densities of LAPW I_(to) decreased slightly less than that of LAA I_(to) in control groups (P > 0.05). After ouabain administration, the current densities of LAPW I_(to) were significantly larger than that of LAA I_(to) [ (10.97±0.58) pA/pF vs (9.39±0.83) pA/pF, P < 0.05]. The I-V curve of LAPW I_(to) was slightly lowered to I-V curve of LAA I_(to) in control groups. But with perfusion of ouabain, the I-V curve of LAPW I_(to) opposed to I-V curve of LAA I_(to) significantly changed from the bottom to the top with the same upward direction. (2) With the voltage clamp protocol of I_(Ca-L), the current densities of LAPW I_(Ca-L) markedly decreased compared with that of LAA I_(Ca-L) in control groups (P < 0.05). With the addition of ouabain, the peak of amplitude of LAPW I_(Ca-L) at +20 mV obviously increased to that of LAA I_(Ca-L) [(-11.13±0.99) pA/ pF vs(-8.86±0.51) pA/pF, P < 0.01]. In the control groups, the I-V curve of LAPW I_(Ca-L) was shifted to the bottom of all I-V curves of I_(Ca-L). Through the effects of ouabain, the I-V curve of LAPW I_(Ca-L) was completely upgraded to the top of other I-V curves of I_(Ca-L). However, all shapes and directions of current peak of I-V curves of I_(Ca-L) remained unchanged in both groups. Conclusion The distribution properties of I_(Ca-L) have significant difference in LAPW. Ouabain can accentuate the electrophysiological heterogeneity and electrical remodeling of I_(to) and I_(Ca-L) in LAPW of rabbits. It may become the triggering factor and persisting basis of AF vulnerability.