The Establishment Of Animal Model Of Persistent Atrial Fibrillation Induced By Rapid Atrial Pacing And Study The Intervention Effects Of Benazepril On It

BackgroundAtrial fibrillation (AF) is one of the most common cardiac arrythmia, is also a main problem in the field in the21st century. Most patients with AF have many comorbidities such as atrial degeneration, tachycardia-induced cardiomyopathy, heart failure, peripheral embolism. The rate of mortality and disability of AF are higher. The pathogenesis of atrial fibrillation remains unclear at present, and the therapeutic effect of traditional treatment is not satisfactory. A large number of studies have shown that the renin-angiotensin-aldosterone system (RAAS) is involved in the formation and maintenance mechanisms of AF, and will indicate a new direction for the treatment of atrial fibrillation. RAAS effector hormone Ang II and Aid promote proliferation and division of ventricular and vascular fibroblast and the synthesis of type Ⅰ, Ⅲ collagen. Therefore, inhibition of RAAS drugs can prevent and reduce the occurrence of AF and has important clinical significance for looking for AF therapy. It is important to study the underlying mechanisms of AF and to identify therapeutic targets. ObjectionTo establish the animal model of persistent atrial fibrillation (AF) and to study the benazepril intervention effects.MethodsThirty New Zealand rabbits (similar weight, male or female), were randomly divided into three groups, the control group (n=10)(pacemaker implantation, but not pacing), the atrial fibrillation model group (n=10)(pacemaker implantation and high frequency pacing the left atrial appendage), benazepril intervention group (n=10)(pacemaker implantation and high frequency pacing the left atrial appendage). All rabbits underwent thoracic surgery, the left atrial appendage epicardial pacing electrode was sutured, the pacemaker embedded in abdominal subcutaneous. The control group did not pace, the atrial fibrillation and benazepril group showed sustained rapid pacing, left atrial appendage formed the atrial fibrillation model. Rabbits in benazepril group was intragastrically administered5mg/(kg·d) benazepril beginning on the day of surgery, the electrocardiogram was observed after4weeks, the control group does not show atrial fibrillation, however, in atrial fibrillation group,10rabbits were persistent atrial fibrillation (AF duration greater than24hours); in benazepril group, only1showed persistent atrial fibrillation. All rabbits in each group were sacrificed after4weeks, atrial muscle tissues were fixed and sectioned for HE staining, and calculated the dissolved ratio, type III collagen was assayed by immunohistochemistry and semi-quantitative analysis. Atrial muscle cell ultrastructural changes were observed under electron microscope.ResultsRabbit persistent atrial fibrillation modeling had a high success rate under high-frequency epicardial pacing the left atrial appendage and it is easy to operate. Dissolution rate of atrial muscle cells in benazepril group was lower than that in atrial fibrillation group (P<0.05), however, there was no significant difference compared to control group (P>0.05). The levels of type III collagen of atrial tissues in benazepril group was significantly lower than those in atrial fibrillation group, while there was no significant difference compared to control group.ConclusionsThe method of establishing rabbit persistent atrial fibrillation model under high-frequency epicardial pacing the left atrial appendage is reliable. Benazepril can block structural remodeling of AF.