We have successfully induced a novel model through a combination of periaortic CaCl2 and elastase incubat

Van-Gieson dye for elastin, and picrosirius red for collagen under conventional light or AbMole Mepiroxol polarized microscopy. Images of the sections were analyzed by using ImageJ 1.41 software as previously described. In the HE-stained sections, the media thickness, intima thickness and intima-media thickness were measured as the average thickness of 10 points of cross-sectional aortic area. Semiquantitative analyses for elastin and collagen content were performed and calculated by measuring the elastin and collagen area in the EVG-stained and PSR-stained sections. The native AAA model induced by elastase perfusion is a standard aneurysm model for experimental research in rodents and rabbits. Anidjar et al. first introduced this method to create an AAA model in rats and suggested that elastase can lead to AAA development through enhanced inflammation response, elastolysis and subsequent destruction of the aortic walls. In this popular model, a catheter is inserted into the femoral artery, the isolated aorta is clamped to block blood circulation and the femoral artery is ligated and subsequently sutured. These procedures make this model more complex and less accessible than models created by adventitial elastolysis that are created by bathing infra-renal aorta segments in elastase solution for 70 min or up to 3 hours. The incubation is obviously lengthy, which might result in high mortality or other failures of the surgical procedure. A CaCl2-induced aneurysm model is another standard aneurysm model in rodents and rabbits. Due to the high affinity of calcium for elastin, calcium deposition within the elastic network of the media can cause the calcium-elastic tissue complex to weaken the vessel wall and develop aneurysm. There is a temporal correlation between inflammatory infiltration and enlargement of aortic aneurysm in vivo. This complex can also serve as the focus of inflammatory, arteriosclerotic reaction of the aortic wall and subsequent aortic aneurysm development. Tanaka et al. developed a novel rat AAA model using a combination of intraluminal elastase infusion and extraluminal CaCl2 exposure. We altered the elastase administration by periaortic incubation and simplified this operation dramatically. Periaortic incubation also avoids contact with blood, which is beneficial because elastase inhibition can be reduced by rabbit serum. Moreover, rabbit aneurysms are suitable for performing endovascular aneurysm repair and for investigating the pharmacologic or gene therapeutic effects from drug-eluting stents or stent graft-mediated gene delivery systems. It is quite obvious that the novel rat AAA model induced by Tanaka et al. is too small to perform aneurysm repair. Zhong et al. successfully implanted partially covered polyester stent grafts in rabbit balloon-injured aortas, and our model will be helpful for further endovascular research by stent graft.