| Summary: | Aortic elastin allows arterial expansion on systole and subsequent elastic recoil during diastole, providing crucial capacitance and associated dampening of the cardiac pressure pulses. The structure and mechanical properties of the aortic wall are not uniform along its length due to the varying hemodynamic conditions to which it is exposed, but elastin’s contributions to this variation are not well studied. The artery wall is a composite of two main structural proteins: elastin and collagen. Autoclaving an intact aorta removes the collagen and produces a mechanically competent vessel consisting of purified elastin, which can be used to study elastin’s contribution to arterial mechanics. Although it is generally assumed that elastin’s material stiffness is constant, a recent study in pigs found that it increased 30% along the thoracic aorta. I hypothesized that this increase in elastin stiffness was caused by a difference in the amount of elastin, the amount or orientation of the interlamellar elastin fibres (IEL), the partitioning of elastin between its three forms, the thickness or orientation of the elastic lamellae, or the number of elastin struts. Uniaxial tensile testing of autoclaved mouse aortas showed that elastin’s stiffness is 43% lower in abdominal aortas compared with thoracic aortas, allowing the mouse aorta to be used as a model to investigate this surprising variation in elastin stiffness. Elastin structure within the thin mouse aortic walls was imaged with multiphoton laser scanning microscopy to identify any differences in the elastin structure that could cause the variation in stiffness. No difference was found between the elastin structure of the thoracic and abdominal aortas that could account for the difference in elastic modulus; however, I was not able to count the elastin struts or measure the elastin fibre packing density in the elastic lamellae and so could not reject these two hypotheses.
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