医学
腹主动脉瘤
血管紧张素II
动脉瘤
弹性蛋白酶
腹主动脉
主动脉瘤
促炎细胞因子
主动脉
内科学
灌注
外科
炎症
血压
生物
酶
生物化学
作者
Jianing Yue,Yin Li,Jian Shen,Zhenjie Liu
标识
DOI:10.1016/j.avsg.2020.03.002
摘要
Background The perfused elastase AAA model and subcutaneous Angiotensin II infusion AAA model are widely used murine AAA models. We modified these two current models and developed a new murine model to study aneurysm formation and rupture. Methods The murine abdominal aorta was treated with elastase. Angiotensin II was infused at a dose of 1,000 ng/kg/min via an osmotic pump placed subcutaneously. A saline osmotic pump was used as the control. The aortas were harvested from the mice 4 weeks later, or earlier if mice died. The abdominal aorta was inspected using ultrasound and microscopy for aneurysm formation and/or signs of rupture. The aneurysm outcome was measured using aortic expansion and proinflammatory cytokine expression. It was also compared with the established conventional elastase perfusion and angiotensin II infusion abdominal aortic aneurysm models. Results By day 28 after surgery, all abdominal aortas of mice treated in the modified group had dilated and progressed to abdominal aortic aneurysms with 60% ruptured aneurysms, whereas none of the control aortas treated with saline became aneurysmal. In mice treated with elastase solution alone, 100% developed aneurysms and only one had a ruptured aneurysm. In mice given angiotensin II infusion alone, 37.5% developed aneurysms and none had a ruptured aneurysm. Histological examination of the modified murine abdominal aortic aneurysm rupture model was identical to that observed in the conventional elastase model. Quantitative polymerase chain reaction analysis revealed similarly increased levels of proinflammatory cytokines. Conclusions We modified two current murine abdominal aortic aneurysm models to develop a murine abdominal aortic aneurysm model with consistent aneurysm formation and high rupture incidence, which can be used for studying abdominal aortic aneurysm rupture and treatment. The perfused elastase AAA model and subcutaneous Angiotensin II infusion AAA model are widely used murine AAA models. We modified these two current models and developed a new murine model to study aneurysm formation and rupture. The murine abdominal aorta was treated with elastase. Angiotensin II was infused at a dose of 1,000 ng/kg/min via an osmotic pump placed subcutaneously. A saline osmotic pump was used as the control. The aortas were harvested from the mice 4 weeks later, or earlier if mice died. The abdominal aorta was inspected using ultrasound and microscopy for aneurysm formation and/or signs of rupture. The aneurysm outcome was measured using aortic expansion and proinflammatory cytokine expression. It was also compared with the established conventional elastase perfusion and angiotensin II infusion abdominal aortic aneurysm models. By day 28 after surgery, all abdominal aortas of mice treated in the modified group had dilated and progressed to abdominal aortic aneurysms with 60% ruptured aneurysms, whereas none of the control aortas treated with saline became aneurysmal. In mice treated with elastase solution alone, 100% developed aneurysms and only one had a ruptured aneurysm. In mice given angiotensin II infusion alone, 37.5% developed aneurysms and none had a ruptured aneurysm. Histological examination of the modified murine abdominal aortic aneurysm rupture model was identical to that observed in the conventional elastase model. Quantitative polymerase chain reaction analysis revealed similarly increased levels of proinflammatory cytokines. We modified two current murine abdominal aortic aneurysm models to develop a murine abdominal aortic aneurysm model with consistent aneurysm formation and high rupture incidence, which can be used for studying abdominal aortic aneurysm rupture and treatment.
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