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Abstract Background Research on the etiology and pathophysiology of fusiform aneurysm has been impeded due to the inability to collect fusiform aneurysm specimens. We aim to resolve this through the development of a novel fusiform aneurysm model in rabbits. Methods Sixty New Zealand White rabbits were divided into ten groups (n = 6 per group): groups A, B, C, D, E and groups a, b, c, d, e. Elastase, at a concentration of 0, 0.5, 1, 2.5 and 5 U/μL respectively was administered to each rabbit to incubate their carotid arteries. Three weeks later, angiography, histomorphometry, immunohistochemistry and immunofluorescent were performed. Results Heparin administration is indispensable. No thrombosis was observed in groups A, B, C, D and E, whereas, increased thromboembolism occurred in groups a, b, c, d and e. Based on the size and wall thickness of aneurysms specimens, 5 U/μL was the optimal concentration of elastase to induce fusiform aneurysms. At 5 U/μL, the intraluminal carotid diameter increased significantly from 2.50 ± 0.32 mm to 3.11 ± 0.55 mm (p < 0.01). The wall thickness significantly reduced from 176.0 ± 39.8 μm to 39.7 ± 14.6 μm (p < 0.01) post aneurysm induction. The histolopathological evaluation revealed the elastic lamina and the smooth muscle cell’s lamina were markedly attenuated and the intimal endothelial lamina became thin or even absent. Conclusions Our research demonstrates that intracranial fusiform aneurysm could be modeled in rabbit carotid artery adventitia incubation by porcine pancreatic elastase.