Arteries can buckle axially under applied critical buckling pressure due to a mechanical instability. Buckling can cause arterial tortuosity leading to flow irregularities and stroke. Genetic mutations in elastic fiber proteins are associated with arterial tortuosity in humans and mice, and may be the result of alterations in critical buckling pressure. Hence, the objective of this study is to investigate how genetic defects in elastic fibers affect buckling pressure. We use mouse models of human disease with reduced amounts of elastin (. Eln+/-) and with defects in elastic fiber assembly due to the absence of fibulin-5 (. Fbln5-/-). We find that Eln+/- arteries have reduced buckling pressure compared to their wild-type controls. Fbln5-/- arteries have similar buckling pressure to wild-type at low axial stretch, but increased buckling pressure at high stretch. We fit material parameters to mechanical test data for Eln+/-, Fbln5-/- and wild-type arteries using Fung and four-fiber strain energy functions. Fitted parameters are used to predict theoretical buckling pressure based on equilibrium of an inflated, buckled, thick-walled cylinder. In general, the theoretical predictions underestimate the buckling pressure at low axial stretch and overestimate the buckling pressure at high stretch. The theoretical predictions with both models replicate the increased buckling pressure at high stretch for Fbln5-/- arteries, but the four-fiber model predictions best match the experimental trends in buckling pressure changes with axial stretch. This study provides experimental and theoretical methods for further investigating the influence of genetic mutations in elastic fibers on buckling behavior and the development of arterial tortuosity.

Original languageEnglish
Pages (from-to)69-82
Number of pages14
JournalJournal of the Mechanical Behavior of Biomedical Materials
StatePublished - Jun 1 2015


  • Elastin
  • Fibulin-5
  • Mechanics
  • Tortuosity


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