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 fus...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.展开更多
文摘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.
