The Establishment Of Experimental Models Of Aortic Dissecting Aneurysm

Objective The purpose is to investigate the method and announcements of establishing an experimental animal model of Debakey typeⅢdissecting aneurysm, which will be more similar to clinical counterparts in morphology, pathology and pathogenesis, so as to provide experimental foundation for the research on the formation and development of dissecting aneurysm, and also to offer reliable animal model and experimental basis for exploring therapeutic ways for treatment.Materials and methods Twelve healthy pigs, 5-7months old, 12-16kg, were randomly divided into high lipidic diet group(n=6) and ordinary diet group(n=6).The data of blood serum total cholesterol, triglyceride, high-density lipoprotein, low-density lipoprotein, apolipoprotein Al, apolipoprotein B were determined before and 4 weeks,8 weeks after feeding, and the corresponding weights were registered as well. All the animals were performed surgical intervention under general anesthesia to establish model of dissecting aneurysm. Elastase, and heparinized normal saline were infused into tunica media of the descending aorta for resolving elastin, in order to separate the tunica media and tunica intima of aortic wall. Then, clamped the infused aorta at both ends and rapidly slit the vessel wall in full-thickness, further separated tunica media and tunica intima, and cut part of tunica intima. The aorta was declamped after suturing tunica media and tunica adventitia. Adrenaline 0.5-1mg was injected intravenously soon to increase blood pressure, for accelerating the stripping of dissection. The diameters of the aorta before and after operation were measured. Anticoagulant were given to prevent thrombogenesis in the dissection. MRI was performed to confirmed the existence of dissection of aorta. Dead animals had autopsy immediately, specimen of descending aorta was examined grossly and microscopically. Datas were expressed as mean±standard deviation. Analysis of variance was used for statistical evaluation. P < 0.05 was considered statistically significant.Results①In high lipidic diet group, the levels of blood serum total cholesterol, low-density lipoprotein, apolipoprotein B rised obviously 4 weeks after feeding (P< 0.01), and more significantly rised 8 weeks later (P < 0.001); there was no significant difference as to the level of triglyceride 4 weeks later (P > 0.05) , but it rised significantly 8 weeks later (P < 0.01) ; the level of high-density lipoprotein rised to some degree 4 and 8 weeks later (P < 0.01, P < 0.001) ,however, the ratio of high-density lipoprotein to total cholesterol and high-density lipoprotein to low-density lipoprotein lowered significantly 8 weeks after feeding (P < 0.01, P < 0.001) . In ordinary diet group, the levels of blood fat were similar before and after feeding. As to weight, there's no significant difference between two groups (P > 0.05). The basic blood pressure of high lipidic diet group were higher than that of ordinary diet group, 190-200/160-170mmHg and 140-150/110-120mmHg respectively.②In high lipidic diet group, 3 animals died and dissecting aneurysm existed in 2 animals. In ordinary diet group, 2 animals died and dissecting aneurysm existed in 1 animal.③The diameters of aorta before operation in high diet group and ordinary diet group were 1.0-1.4cm,0.9-1.3cm respectively, and after operation 1.8-2.2cm,1.6-1.8cm respectively.④Gross appearance showed the crevasse of tunica intima and the separation between tunica media and tunica intima. The walls of aneurysms were thin and weak. In high lipidic diet group, pathological research had found the eminence,deformation of endothelial tissue, and a scanty lipochondria depositing in tunica intima. Inflammatory cells could be found. Layers of elastic fibers were found to obviously decrease or interrupt with Weigert stain. There were no abnormal findings in ordinary diet group.Conclusions①The injury of aortic tunica intima results in the crevasse, through which the blood passes into tunica media and separates the aortic wall under high pressure, forming hematoma that further strips and expands, thus producing the pseudocoele and aortic dissecting aneurysm. The cataplasia of medical elastic fibers and medical cystic necrosis are pathological foundations for this disease, which commonly caused by hypertensive disease and artherosclerosis.②This method to establish animal model is corresponding with the pathological foundations and pathogenesis of dissecting aneurysm, which is scientific and feasible.③High lipidic diet given before operation for a certain period can produce hyperlipemia. Both the basic blood pressure heightens and the aorta in early stage of sclerosis, are corresponding with the pathological foundations of dissecting aneurysm. Elastase has resolved elastic fibers and relieved the elastic recovery effects, which may be beneficial to the expansion of aneurysm.④This method can provide reliable animal model and experimental basis for diagnosing disease and exploring new therapeutic ways for aortic dissecting aneurysm.