Bersi M R, Collins M J, Wilson E, Humphrey J D
Department of Biomedical Engineering, Yale University, New Haven, CT, USA.
Department of Biomedical Engineering, Texas A&M University, College Station, TX, USA.
Int J Adv Eng Sci Appl Math. 2013 Dec 1;4(4):228-240. doi: 10.1007/s12572-012-0052-4.
Chronic infusion of angiotensin-II has proved useful for generating dissecting aortic aneurysms in atheroprone mice. These lesions preferentially form in the suprarenal abdominal aorta and sometimes in the ascending aorta, but reasons for such localization remain unknown. This study focused on why these lesions do not form in other large (central) arteries. Toward this end, we quantified and compared the geometry, composition, and biaxial material behavior (using a nonlinear constitutive relation) of common carotid arteries from three groups of mice: non-treated controls as well as mice receiving a subcutaneous infusion of angiotensin-II for 28 days that either did or did not lead to the development of a dissecting aortic aneurysm. Consistent with the mild hypertension induced by the angiotensin-II, the carotid wall thickened as expected and remodeled modestly. There was no evidence, however, of a marked loss of elastic fibers or smooth muscle cells, each of which appear to be initiating events for the development of aneurysms, and there was no evidence of intramural discontinuities that might give rise to dissections.
事实证明，长期输注血管紧张素 II 有助于在易患动脉粥样硬化的小鼠中诱发主动脉夹层动脉瘤。这些病变优先出现在肾上腺上方的腹主动脉，有时也出现在升主动脉，但这种定位的原因尚不清楚。本研究聚焦于为何这些病变不在其他大（中央）动脉中形成。为此，我们对三组小鼠的颈总动脉的几何形状、组成和双轴材料行为（使用非线性本构关系）进行了量化和比较：未治疗的对照组以及皮下输注血管紧张素 II 28 天的小鼠，后者有的发生了主动脉夹层动脉瘤，有的未发生。与血管紧张素 II 诱发的轻度高血压一致，颈动脉壁如预期那样增厚并适度重塑。然而，没有证据表明弹性纤维或平滑肌细胞明显丢失，而这两者似乎都是动脉瘤形成的起始事件，也没有证据表明存在可能导致夹层的壁内连续性中断。
