Yonghua Bi1, Hongshan Zhong2, Ke Xu3, Xun Qi2, Zhen Zhang4, Gang Wu5, Xinwei Han5. 1. Department of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China; Department of Radiology, The First Affiliated Hospital of China Medical University, Shenyang, China; Key Laboratory of Diagnostic Imaging and Interventional Radiology of Liaoning Province, Shenyang, China. 2. Department of Radiology, The First Affiliated Hospital of China Medical University, Shenyang, China; Key Laboratory of Diagnostic Imaging and Interventional Radiology of Liaoning Province, Shenyang, China. 3. Department of Radiology, The First Affiliated Hospital of China Medical University, Shenyang, China; Key Laboratory of Diagnostic Imaging and Interventional Radiology of Liaoning Province, Shenyang, China. Electronic address: kexu@vip.sina.com. 4. Key Laboratory of Diagnostic Imaging and Interventional Radiology of Liaoning Province, Shenyang, China; Department of Ultrasound, The First Affiliated Hospital of China Medical University, Shenyang, China. 5. Department of Interventional Radiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Abstract
OBJECTIVE: This study tested the hypothesis that an experimental model of abdominal aortic aneurysm in rabbits results in progressive enlargement when induced by a combination of periaortic elastase administration and aortic coarctation. METHODS: Male New Zealand white rabbits were randomly divided into four groups: (A) stenosis (n = 12), (B) elastase (n = 12), (C) aneurysm (n = 15), and (D) control (n = 12). The stenosis group received an extrinsic coarctation below the right renal artery, the elastase group received a 10-minute administration of 60 μL elastase (1 U/μL) in a 1.5-cm aortic segment, the aneurysm group received stenosis and elastase, and a sham operation was performed in the control group. The aortic diameter was measured after 1, 2, 4, 8, and 16 weeks, and animals were subsequently euthanized for histopathologic and immunohistochemical studies. RESULTS: All animals in the aneurysm group developed aneurysm by 2 weeks after treatment, with average diameters of 5.21 ± 0.74 mm by 2 weeks, 6.23 ± 1.10 mm by 4 weeks, 7.87 ± 0.50 mm by 8 weeks, and 9.40 ± 0.36 mm by 16 weeks. Aortic diameter dilated progressively, and all aneurysms developed by 4 weeks in the stenosis group (4.17 ± 0.22 mm). Only one aneurysm was seen in the elastase group by week 1 (3.60 ± 0.64 mm), and no aneurysm formed in the control group by week 8 (2.47 ± 0.38 mm). The aneurysm group exhibited less media thickness, elastin content, and endothelial recovery, but stronger expression of matrix metalloproteinase 2 and 9 and rabbit macrophage compared with the control group. CONCLUSIONS: This novel rabbit abdominal aortic aneurysm model with a gradually enlarging diameter is simply and reliably induced, appropriately mimicking human aortic aneurysm disease.
OBJECTIVE: This study tested the hypothesis that an experimental model of abdominal aortic aneurysm in rabbits results in progressive enlargement when induced by a combination of periaortic elastase administration and aortic coarctation. METHODS: Male New Zealand white rabbits were randomly divided into four groups: (A) stenosis (n = 12), (B) elastase (n = 12), (C) aneurysm (n = 15), and (D) control (n = 12). The stenosis group received an extrinsic coarctation below the right renal artery, the elastase group received a 10-minute administration of 60 μL elastase (1 U/μL) in a 1.5-cm aortic segment, the aneurysm group received stenosis and elastase, and a sham operation was performed in the control group. The aortic diameter was measured after 1, 2, 4, 8, and 16 weeks, and animals were subsequently euthanized for histopathologic and immunohistochemical studies. RESULTS: All animals in the aneurysm group developed aneurysm by 2 weeks after treatment, with average diameters of 5.21 ± 0.74 mm by 2 weeks, 6.23 ± 1.10 mm by 4 weeks, 7.87 ± 0.50 mm by 8 weeks, and 9.40 ± 0.36 mm by 16 weeks. Aortic diameter dilated progressively, and all aneurysms developed by 4 weeks in the stenosis group (4.17 ± 0.22 mm). Only one aneurysm was seen in the elastase group by week 1 (3.60 ± 0.64 mm), and no aneurysm formed in the control group by week 8 (2.47 ± 0.38 mm). The aneurysm group exhibited less media thickness, elastin content, and endothelial recovery, but stronger expression of matrix metalloproteinase 2 and 9 and rabbit macrophage compared with the control group. CONCLUSIONS: This novel rabbitabdominal aortic aneurysm model with a gradually enlarging diameter is simply and reliably induced, appropriately mimicking humanaortic aneurysm disease.
Authors: Uwe Raaz; Alexander M Zöllner; Isabel N Schellinger; Ryuji Toh; Futoshi Nakagami; Moritz Brandt; Fabian C Emrich; Yosuke Kayama; Suzanne Eken; Matti Adam; Lars Maegdefessel; Thomas Hertel; Alicia Deng; Ann Jagger; Michael Buerke; Ronald L Dalman; Joshua M Spin; Ellen Kuhl; Philip S Tsao Journal: Circulation Date: 2016-01-05 Impact factor: 29.690