适合腔内治疗的兔新型腹主动脉瘤模型建立及血流动力学对新模型的作用及机制

Complications such as endoleak and stent migration greatly reduce the mid or long-term curative effect of endovascular aortic repair (EVAR) for abdominal aortic aneurysm (AAA). Deficient biological healing between the covered stent and target vessel is the main cause of complications. Porcine or canine AAA models, induced for EVAR studies, are unable to investigate the biological healing, due to the dramatic difference to human AAA disease. Our previous experiment indicated that rabbit AAA induced by elastase heals spontaneously, matrix metalloproteases may play a positive role in the complex aortic remodeling of AAA, and hemodynamics is vital to the formation and progression of AAA. Thus, we hypothesize that novel AAA suitable for EVAR and biological healing study can be induced if previous model is modifid by absorbable suture and coarctation is removed by balloon dilation. To test this hypothesis, we will use absorbable suture to optimize our previously induced novel AAA model, and remove the coarctation by balloon dilation to perform EVAR 4 weeks later, avoiding the impact of self-healing on the evaluation of biological healing. EVAR will be performed in optimized novel model, to evaluate biological healing and to study the role of hemodynamics and matrix metalloproteases in novel AAA, and provide novel model for EVAR and new ideal for study of pathogenesis of AAA.

腔内治疗后支架移位及内漏等并发症大大降低了中远期疗效，覆膜支架与靶血管缺乏生物学愈合是引起并发症的重要原因。猪、犬等供腔内治疗研究的模型，病理学与人动脉瘤相差甚远，不太适用于生物学愈合的研究。我们前期实验表明，蛋白酶诱导的兔传统模型可自我修复，基质金属蛋白酶可能在动脉瘤重塑中起积极作用，而血流动力学对动脉瘤发生、发展至关重要。为此，我们提出假说：以可吸收缝合线优化建模，采用球囊扩张解除狭窄可建立适合腔内治疗及生物学愈合评价的模型，且狭窄解除前后血流改变影响动脉瘤发展。为验证这一假说，我们在前期研究基础上，采用可吸收缝合线部分结扎，4周后球囊扩张解除狭窄以通过支架系统，避免模型自我修复对生物学愈合评价的影响。本研究采用优化的新模型进行腔内治疗，初步研究生物学愈合，初步探讨血流动力学和基质金属蛋白酶在新模型中的作用及可能的机制，为腔内治疗提供新的动脉瘤模型，为动脉瘤发生机制的研究提供新思路。

我们前期实验表明，蛋白酶诱导的兔传统腹主动脉瘤（AAA）模型可自我修复，基质金属蛋白酶可能在AAA重塑中起积极作用，而血流动力学对AAA发生、发展至关重要。本研究采用可吸收缝合线部分结扎，4周后球囊扩张解除狭窄以通过支架系统，避免模型自我修复对生物学愈合评价的影响。成功建立适合腔内治疗及生物学愈合评价的AAA模型，并对狭窄解除前后血流改变对AAA的转归进行了研究。综上结果，本研究采用优化的新模型进行腔内治疗，研究生物学愈合，并探讨血流动力学和基质金属蛋白酶的作用及可能的机制，为腔内治疗提供了一种新的AAA模型，为AAA发生机制的研究提供新思路。本项目资助发表论文16篇，SCI论文13篇，中文论文2篇，实用新型专利5项。培养硕士生4名，其中1名已发表1篇SCI论文。项目投入经费18万元，支出16.8773万元，各项支出基本与预算相符，剩余经费1.1227万元，剩余经费及自筹经费将用于本项目研究后续支出。

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