心房纤颤模型电生理及病理学的研究

Electrophysiological and pathological characteristics of a new canine model of atrial fibrillation

目的:建立良好的与临床病理基础相一致的心房纤颤(Af)动物模型,研究其电生理和病理特点.方法:经25只实验犬左上肺静脉置入自制腱索钩刀钩断部分二尖瓣腱索,造成中度二尖瓣返流,术后12wk内,每2wk行1次超声心动图和电生理检查,检查后用Burst刺激法诱发Af.术后第10wk随机取11只实验犬心房肌标本行病理检查.结果:术后2wk左房前后径(mm)增加[(22.7±2.3)vs(20.4±3.1),P<0.05].术后4wkP波时限(ms)延长[(61.0±5.1)vs(48.7±8.8),P<0.01],高位右房有效不应期缩短[(102.7±11.0)vs(133.3±14.9),P<0.01].术后12wk80%(8/10)实验犬诱发出持续时间>5min的Af.病理证实实验犬心房肌细胞肥大,肌原纤维病变,间质纤维化为主要特点.结论:本模型建立方法成功率高,可靠且简单易行,动物实验发现左房扩张、右房有效不应期缩短,心房内传导时间延长,心肌细胞肥大、间质纤维化导致心肌兴奋传导及心肌细胞电生理特性异常,与临床上瓣膜病引起的Af有一定的对应性,是研究Af的良好模型.

AIM： To establish a new animal model of atrial fibrillation（A f） by operation,and to observe the electrophysiological and pathological changes of its atria. METHODS： A specially self-designed hook was introduced into the left atrium of 25 mongrel dogs from the left superior pulmonary vein, and partial chordae endings of mitral valve were transected to produce moderate mitral regurgitation. Echocardiagraphic and electrophysiological study was performed every 2 weeks within 12 weeks postoperatively and Af was induced by burst pacing. Specimens were taken from the atrial myocardium of 11 dogs and observed by using special staining 10 weeks after operation. RESULTS： Anteroposterior dimension of left atrium increased significantly 2 weeks after operation[（22.7±2.3） mmvs （20.4±3.1） mm, P〈0.05]. P wave duration in lead 11 of surface electrocardiography increased from （48.7±8.8） ms to （61.0 ±5.1） ms （P〈0.01）, and effective refractory period of high right atrium（HRA-ERP） decreased from （133.3±14.9） ms to （102.7±11.0） ms （P〈0.01）. Af lasting more than 5 minutes was induced in 80% （8/10）dogs 12 weeks after operation. The changes of myocardium in left atria of experimental group was obvious, and the chief manifestations consisted of hypertrophy, myofibrillar changes, and interstitial fibrosis. CONCLUSION： This model of Af proves to be reliable, reproducible. After operation, the left atrium of animals dilates, HRA-ERP decreases, P wave duration increases. Mycardial hypertrophy and interstitial fibrosis lead to alteration of impulse conduction and changes of myocardial electrophsiological properties.