Aristotelis Agianniotis1, Nikos Stergiopulos. 1. Laboratory of Hemodynamics and Cardiovascular Technology, Institute of Bioengineering, Ecole Polytechnique Fédérale de Lausanne, BM 5128 (Bâtiment BM), Station 17, 1015 Lausanne, Switzerland. aristotelis.agianniotis@epfl.ch
Abstract
OBJECTIVES: We quantified the dysfunction of the aortic wall, determined structural and elastic properties, and provided histological data of the thoracic aortas of apolipoprotein E (apoE)-deficient mice which are used as model of atherosclerosis. METHODS: Six young 10-12 week-old (apoE)-deficient mice of both sexes were studied and six age-matched C57BL/6J wild-type mice were used as control group. We performed extension-inflation mechanical tests at three different axial stretches (λ(z) = 1.6, 1.8, and 2.0), under maximally contracted or totally relaxed state of the vascular smooth muscle cells. Classical histology was performed to the arterial segments. RESULTS: Control aortas were generally more distensible than the (apoE)-deficient mouse aortas under both relaxed and contracted smooth muscle. Also, aortas from (apoE)-deficient mice were stiffer (higher incremental elastic modulus) than control aortas. Control aortas exhibited a higher active diameter response compared to (apoE)-deficient mouse aortas, despite the fact that vascular smooth muscle cell density was increased by approximately 15% in the (apoE)-deficient mouse aortas. CONCLUSION: We found substantial changes in the structural and elastic properties of the wall, in the active diameter response and in the histology of (apoE)-deficient mouse aortas compared to the control group. Our data can be used in the development of constituent-based models of the arterial wall and in studying the changes in arterial wall properties in presence of disease, such as atherosclerosis.
OBJECTIVES: We quantified the dysfunction of the aortic wall, determined structural and elastic properties, and provided histological data of the thoracic aortas of apolipoprotein E (apoE)-deficient mice which are used as model of atherosclerosis. METHODS: Six young 10-12 week-old (apoE)-deficient mice of both sexes were studied and six age-matched C57BL/6J wild-type mice were used as control group. We performed extension-inflation mechanical tests at three different axial stretches (λ(z) = 1.6, 1.8, and 2.0), under maximally contracted or totally relaxed state of the vascular smooth muscle cells. Classical histology was performed to the arterial segments. RESULTS: Control aortas were generally more distensible than the (apoE)-deficient mouse aortas under both relaxed and contracted smooth muscle. Also, aortas from (apoE)-deficient mice were stiffer (higher incremental elastic modulus) than control aortas. Control aortas exhibited a higher active diameter response compared to (apoE)-deficient mouse aortas, despite the fact that vascular smooth muscle cell density was increased by approximately 15% in the (apoE)-deficient mouse aortas. CONCLUSION: We found substantial changes in the structural and elastic properties of the wall, in the active diameter response and in the histology of (apoE)-deficient mouse aortas compared to the control group. Our data can be used in the development of constituent-based models of the arterial wall and in studying the changes in arterial wall properties in presence of disease, such as atherosclerosis.
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