药物诱导联合流出道缩窄构建兔腹主动脉瘤模型的实验研究

Objective: To investigate the feasibility and effectiveness of creating rabbit abdominal aortic aneurysm (AAA) model by using drug induction plus abdominal aortic outflow coarctation. Methods: Twenty-four female New Zealand white rabbits were equally randomized into 4 groups, in which, AAA model was induced by wrapping and infiltrating the vessel with a cotton strip containing a solution of CaCl₂ (0.75 mol/L) or trypsin (0.04 g/mL) in two groups, and the model was constructed by CaCl₂ or trypsin infiltration plus abdominal aorta outflow constriction (50% 60% constriction) in the other two groups. After the operation, the change in diameter of the affected blood vessel was monitored by veterinary ultrasound. The experimental animals were sacrificed 2 weeks after the operation, and the injured abdominal aorta was harvested to prepare tissue sections for HE and EVG staining. The effect of outflow tract coarctation on AAA formation was evaluated by computer simulation. Results: Ultrasound examination on 2 weeks after operation showed that no evident dilatation of the affected vessel was seen, and no vessel reached the standard of AAA formation in the two groups undergoing drug infiltration alone; the affected vessel was obviously dilated in the two group undergoing drug infiltration plus abdominal aortic outflow coarctation, in which, the AAA formation rate was 66.67 % (4/6) in CaCl₂ plus coarctation group, with an average 1.61-fold expansion, and the AAA formation rate was 83.33% (5/6) in trypsin plus coarctation group, with an average 1.89-fold expansion. Compared with the normal abdominal aorta, the thickness of abdominal aorta intima was significantly increased after CaCl₂ infiltration (both P<0.05), but the thickness of abdominal aorta intima did not significantly change after trypsin infiltration (both P>0.05); the thickness of the tunica media was significantly increased and the percentage of the area occupied by the elastic fibers was significantly reduced in all groups, and these changes were most evident in CaCl₂ plus coarctation group (all P<0.05). Computer numerical simulation demonstrated that the vascular wall stress increased and the AAA formation rate increased after the outflow coarctation. Conclusion: Drug induction plus abdominal aortic outflow coarctation can successfully establish the AAA model in rabbits, and shorten the time for model generation. Moreover, the modelling method of trypsin infiltration combined with abdominal aortic outflow coarctation is superior to that of CaCl₂ infiltration combined with abdominal aortic outflow coarctation.