Between the symptoms, psychological factors, duration and altered cerebral structures, the demonstration of gray matter morphometric alterations in the meal-related FD patients could provide a new approach to future studies and give direction to new therapy development. Abdominal aortic aneurysm, defined as a permanent localized aortic dilation with a diameter of 1.5 times the normal aorta diameter, is a silent degenerative disease that can be lifethreatening. Although human AAA is histologically characterized by adventitial inflammation, medial attenuation, elastic fiber destruction and subsequent dilation, the pathogenesis of AAA is not completely understood. Therefore, it is critical to develop reliable and reproducible experimental models to study AAA pathogenesis and to mimic clinical scenarios for translational research. Several small animal models have been developed to assist in understanding the mechanisms of AAA pathogenesis. Anidjar et al. first introduced 
an elastase-induced AAA, one of the most commonly used models in rats. This model requires insertion of a cannula and blockage of blood circulation during an extended elastase perfusion, making the surgical procedure difficult and complex. Periarterial elastase incubation is also used to create an aneurysm in the carotid and aortic arteries in small animals. However, a lengthy elastase incubation in these models may lead to high mortality of the animals and failure of the surgical procedure. Origuchi et al. also noted that periarterial elastase-induced AAA heals spontaneously. The CaCl2-induced AAA model, which was first introduced by Gertz et al. in the rabbit carotid artery and was subsequently used in the aortic artery, is another popular model. Unfortunately, periaortic CaCl2 application does not always induce reliable AAA formation. Isenburg et al. reported that only 8 of 12 rats developed aneurysm, even using an arbitrary threshold of a 20% diameter increase to define AAA. Tanaka et al. introduced a novel rat AAA model induced by a combination of intraluminal elastase infusion and extraluminal CaCl2 exposure. However, this model is still complex because of the insertion of an SP10 polyethylene catheter into the femoral artery, and rabbits are more suitable than rats for investigating the pharmacologic or gene therapeutic effects of drug-eluting stents and stent graft-mediated gene delivery systems. The purpose of this study was to investigate whether a combination of periaortic CaCl2 and elastase incubation could work in concert to develop suitable AAA formation in rabbits. Five and thirty days after surgery, a second laparotomy was performed after imaging and a catheter was then introduced into the abdominal aorta at the level of the renal arteries. After euthanasia by intravenous injection of an overdose of sodium pentobarbital, pressure perfusion fixed with 10% buffered paraformaldehyde solution was processed.