兔心力衰竭时跨室壁复极离散度和缝隙连接蛋白43变化的研究
Changes of transmural dispersion of repolarization and connexin 43 in rabbits with heart failure
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摘要: 目的:探讨阿霉素诱导的兔心力衰竭(heart failure,HF)时跨室壁离散度和缝隙连接蛋白43的变化。方法:将18只日本大耳白兔随机分为对照组(n=10)及模型组(n=8)。采用阿霉素诱导建立兔HF模型。采用单相动作电位(monophasic action potential,MAP)记录技术,分别记录HF组和对照组左室心肌内、中、外膜的MAP,分别测量获得20列三层心室肌的90%动作电位时程(monophasic action potential duration,MAPD90),计算并分析跨室壁复极离散度(transmural dispersity of repolarization,TDR)的变化,TDR为每列中MAPD90 max与MAPD90 min的差值。应用免疫荧光染色法检测缝隙连接蛋白43(gap junction connexin43,CX43)在心肌细胞间分布的变化。结果:与对照组比较HF组的MAPD90缩短,TDR则明显增大(P<0.05)。免疫荧光染色法检测显示,HF组CX43分布与对照组有所差别。结论:HF组心脏TDR增加,CX43分布发生改变,其可能与HF时恶性心律失常的发生有关。Abstract: AIM: To investigate the the changes of transmural dispersion of repolarization(TDR) and connexin 43 in rabbit heart failure.METHODS: Models of adriamycin-induced heart failure were established in rabbits and picardial,mid-and endometrial monophasic action potentials(MAP) in the left ventricular myocardium were recorded with MAP recording technology.Monophasic action potential duration MAPD90 was measured,changes of TDR were analyzed,and distribution changes of gap junction connexin 43(CX43) in the myocardial cells were observed by immunofluorescence.RESULTS: Compared with those in the control group,MAPD90 in the heart failure group was shortened and TDR significantly increased(P<0.05).Immunofluorescence showed differences in CX43 distribution between heart failure group and control group.CONCLUSION: Increased TDR and distribution changes of CX43 in heart failure may be related to occurrence of malignant ventricular arrhythmia.
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