000161732 001__ 161732
000161732 005__ 20181203022238.0
000161732 0247_ $$2doi$$a10.1152/ajpheart.01108.2006
000161732 022__ $$a0363-6135
000161732 02470 $$2PMID$$a17237244
000161732 02470 $$2ISI$$a000247777300025
000161732 037__ $$aARTICLE
000161732 245__ $$aEffect of elastin degradation on carotid wall mechanics as assessed by a constituent-based biomechanical model
000161732 260__ $$c2007
000161732 269__ $$a2007
000161732 336__ $$aJournal Articles
000161732 520__ $$aArteries display a nonlinear anisotropic behavior dictated by the elastic properties and structural arrangement of its main constituents, elastin, collagen, and vascular smooth muscle. Elastin provides for structural integrity and for the compliance of the vessel at low pressure, whereas collagen gives the tensile resistance required at high pressures. Based on the model of Zulliger et al. (Zulliger MA, Rachev A, Stergiopulos N. Am J Physiol Heart Circ Physiol 287: H1335-H1343, 2004), which considers the contributions of elastin, collagen, and vascular smooth muscle cells (VSM) in an explicit form, we assessed the effects of enzymatic degradation of elastin on biomechanical properties of rabbit carotids. Pressure-diameter curves were obtained for controls and after elastin degradation, from which elastic and structural properties were derived. Data were fitted into the model of Zulliger et al. to assess elastic constants of elastin and collagen as well as the characteristics of the collagen engagement profile. The arterial segments were also prepared for histology to visualize and quantify elastin and collagen. Elastase treatment leads to a diameter enlargement, suggesting the existence of significant compressive prestresses within the wall. The elastic modulus was more ductile in treated arteries at low circumferential stretches and significantly greater at elevated circumferential stretches. Abrupt collagen fiber recruitment in elastase-treated arteries leads to a much stiffer vessel at high extensions. This change in collagen engagement properties results from structural alterations provoked by the degradation of elastin, suggesting a clear interaction between elastin and collagen, often neglected in previous constituent-based models of the arterial wall.
000161732 6531_ $$aMechanotransduction, Cellular
000161732 6531_ $$aModels, Cardiovascular
000161732 700__ $$aFonck, E
000161732 700__ $$aProd'hom, G
000161732 700__ $$0246199$$aRoy, S$$g157387
000161732 700__ $$aAugsburger, L
000161732 700__ $$aRüfenacht, D A
000161732 700__ $$0240635$$aStergiopulos, N$$g106482
000161732 773__ $$j292$$k6$$qH2754-63$$tAmerican journal of physiology. Heart and circulatory physiology
000161732 909C0 $$0252351$$pLHTC$$xU11843
000161732 909CO $$ooai:infoscience.tind.io:161732$$pSTI$$particle
000161732 937__ $$aEPFL-ARTICLE-161732
000161732 973__ $$aEPFL$$rREVIEWED$$sPUBLISHED
000161732 980__ $$aARTICLE