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Abstract：
OBJECTIVE: To understand the anatomy and physiology of ascending aortic aneurysms in angiotensin II-infused ApoE(-/-) mice.
RESULTS: We combined an extensive in vivo imaging protocol (high-frequency ultrasound and contrast-enhanced microcomputed tomography at baseline and after 3, 10, 18, and 28 days of angiotensin II infusion) with synchrotron-based ultrahigh resolution ex vivo imaging (phase contrast X-ray tomographic microscopy) in n=47 angiotensin II-infused mice and 6 controls. Aortic regurgitation increased significantly over time, as did the luminal volume of the ascending aorta. In the samples that were scanned ex vivo, we observed one or several focal dissections, with the largest located in the outer convex aspect of the ascending aorta. The volume of the dissections moderately correlated to the volume of the aneurysm as measured in vivo (r(2)=0.46). After 3 days of angiotensin II infusion, we found an interlaminar hematoma in 7/12 animals, which could be linked to an intimal tear. There was also a significant increase in single laminar ruptures, which may have facilitated a progressive enlargement of the focal dissections over time. At later time points, the hematoma was resorbed and the medial and adventitial thickness increased. Fatal transmural dissection occurred in 8/47 mice at an early stage of the disease, before adventita remodeling.
CONCLUSIONS: We visualized and quantified the dissections that lead to ascending aortic aneurysms in angiotensin II-infused mice and provided unique insight into the temporal evolution of these lesions.
RESULTS: We combined an extensive in vivo imaging protocol (high-frequency ultrasound and contrast-enhanced microcomputed tomography at baseline and after 3, 10, 18, and 28 days of angiotensin II infusion) with synchrotron-based ultrahigh resolution ex vivo imaging (phase contrast X-ray tomographic microscopy) in n=47 angiotensin II-infused mice and 6 controls. Aortic regurgitation increased significantly over time, as did the luminal volume of the ascending aorta. In the samples that were scanned ex vivo, we observed one or several focal dissections, with the largest located in the outer convex aspect of the ascending aorta. The volume of the dissections moderately correlated to the volume of the aneurysm as measured in vivo (r(2)=0.46). After 3 days of angiotensin II infusion, we found an interlaminar hematoma in 7/12 animals, which could be linked to an intimal tear. There was also a significant increase in single laminar ruptures, which may have facilitated a progressive enlargement of the focal dissections over time. At later time points, the hematoma was resorbed and the medial and adventitial thickness increased. Fatal transmural dissection occurred in 8/47 mice at an early stage of the disease, before adventita remodeling.
CONCLUSIONS: We visualized and quantified the dissections that lead to ascending aortic aneurysms in angiotensin II-infused mice and provided unique insight into the temporal evolution of these lesions.
摘要：
目的：了解输入血管紧张素II的ApoE（-/-）小鼠升主动脉瘤的解剖和生理学。
结果：我们将广泛的体内成像方案（在基线和输注血管紧张素II3、10、18和28天后的高频超声和对比增强显微计算机断层扫描）与基于同步加速器的超高分辨率离体成像（相衬X射线断层显微镜）结合在n=47只输注血管紧张素II的小鼠和6只对照中。主动脉瓣反流随时间显著增加,升主动脉的腔容积也是如此。在离体扫描的样本中，我们观察到一个或几个局灶性解剖，最大的位于升主动脉的外凸面。解剖的体积与体内测量的动脉瘤的体积适度相关（r（2）=0.46）。输注血管紧张素II3天后，我们在7/12只动物中发现了层间隙血肿,这可能与内膜撕裂有关.单个层状破裂也显着增加，随着时间的推移，这可能促进了病灶解剖的逐渐扩大。在稍后的时间点，血肿被吸收，内侧和外膜厚度增加。致命的透壁解剖发生在8/47小鼠在疾病的早期阶段，在外胚层重塑之前。
结论：我们可视化并量化了血管紧张素II输注小鼠中导致升主动脉瘤的夹层，并提供了对这些病变的时间演变的独特见解。
结果：我们将广泛的体内成像方案（在基线和输注血管紧张素II3、10、18和28天后的高频超声和对比增强显微计算机断层扫描）与基于同步加速器的超高分辨率离体成像（相衬X射线断层显微镜）结合在n=47只输注血管紧张素II的小鼠和6只对照中。主动脉瓣反流随时间显著增加,升主动脉的腔容积也是如此。在离体扫描的样本中，我们观察到一个或几个局灶性解剖，最大的位于升主动脉的外凸面。解剖的体积与体内测量的动脉瘤的体积适度相关（r（2）=0.46）。输注血管紧张素II3天后，我们在7/12只动物中发现了层间隙血肿,这可能与内膜撕裂有关.单个层状破裂也显着增加，随着时间的推移，这可能促进了病灶解剖的逐渐扩大。在稍后的时间点，血肿被吸收，内侧和外膜厚度增加。致命的透壁解剖发生在8/47小鼠在疾病的早期阶段，在外胚层重塑之前。
结论：我们可视化并量化了血管紧张素II输注小鼠中导致升主动脉瘤的夹层，并提供了对这些病变的时间演变的独特见解。
