建立犬心房颤动模型的研究

用自制健索钩刀破坏25条犬部分二尖瓣腱索，造成中等程度二尖瓣关闭不全，建立心房颤动（AF）动物模型。术后12周内每2周1次行超声心动图及电生理检查，每次检查后用Burst刺激法诱发AF。术后2周左房前后径增加（22．70±2．31mmvs20．39±3．08mm，P＜0．05），术后4周左房面积增加（7．01±1．91cm2vs5．63±2．05cm2，P＜0．05）。术后4周P波时限延长（61．00±5．07msvs48．75±8．82ms）、高位右房有效不应期缩短（102．67±11．00msvs133．33±14．97ms），P均＜0．01。术后12周80％（8／10）的犬可诱发出持续时间＞5min的AF。左、有房AF波周期无显著差异（102．50±17．89msvs116．60±18．24ms，P＞0．05）。通过破坏二尖瓣腱索造成犬急性二尖瓣关闭不全，手术后随时间延长，动物表现在房扩张及右房有效不应期缩短和心房内传导时间延长，此与临床上瓣膜病引起的AF有一定的对应性，因而是研究AF电生理的良好模型。

Study on the Establishment of A Canine Model of Atrial Fibrillation

An identical animal model is necessary to study the electrophysiological mechanisms of atrial fibrillation(AF) and its treatment. In this experiment,a canine model of AP was established in 25 mongrel dogs by destroyingpartial chordae tendinese with a self-designed hook. Moderate mitral regurgitation was caused after chordaetendineae destroying,which serves as the pathological mechanism of this AF model. Echocardiagraphic and electro-physiological study was performed every two weeks in 12 weeks postoperatively and AF was induced by burst pac-ing after each examination. Anterposterior dimension of left atrium (LA) increased significantly two weeks afteroperation (22. 70± 2. 31 mm vs 20. 39± 3. 08 mm,P<0.05),LA area increased significantly 4 weeks after opera-tion (7. 01±1. 91 cm2 vs 5. 63±2. 05 cm2,P<0. 05). P wave duration in lead, Ⅱ of surface electrocardiography in-creased from 48. 75 ± 8. 82 ms to 61. 00 ±5. 07 ms (P<0. 01 ), effective refractory period of high right atrium(HRA-ERP) decreased from 133.33±14. 97 ms to 102.67± 11. 00 ms (P<0.01). AF lasting more than 5 minutescould be induced in 80% (8/10) dogs 12 weeks after operation. No significant difference was found between atrialfibrillation cycle lengths (AFCLs) of two atrial .Though mitral rigUrgitation caused by destroving chordae tendiaeawas an acute one, after operation the left atrium of animals dialated, HRA-ERP decreased, P wave duration in-creased,thus the pathological and electrophysiological characterization of this model is similar with that of clinicalpatients with AF caused by valvuer disease,this model is a valuable one relevent to AF of rheumatic valvuer dis-ease.