Defining Multiscale, Rate-Dependent Damage Mechanisms in Blood Vessels

University Of Utah, Salt Lake City UT

Investigators

Abstract

Blood vessels can be damaged as a result of large shape changes – deformations – that occur in both accidents (such as traumatic brain injury) and surgery (such as angioplasty). However, little is known about how this damage affects a vessel’s ability to continue to perform its function. This is especially true when damage is subtle and there is no bleeding. Additionally, recent research shows that the rate of deformation influences the type of resulting damage. The goals of this project are to define damage mechanisms in blood vessels and to define how damage changes vessel function. The project focuses on blood vessels in the brain. The results of this project will provide insight about damage mechanisms in traumatic brain injury, and may eventually lead to better healthcare treatments. This information will improve design criteria for automobiles, helmets, and other protective devices. It may also reveal factors that increase the risk of stroke after brain injury. It may also improve outcomes of balloon angioplasty procedures. Researchers involved in this project will include students from underrepresented groups, who will gain valuable professional development. The aims of this project are (1) to differentiate and quantify contributions of both recoverable (e.g. viscoelasticity) and non-recoverable (e.g. collagen unfolding) mechanisms of vessel softening, and (2) to define the influence of strain rate on mechanisms of damage. Microstructural damage and associated softening will be defined using isolated blood vessels subjected to overstretch through a range of strain rates. Experimental findings will be incorporated into a novel constitutive model that relates multiscale damage of passive vessel constituents with mechanical behavior. This is a critical first step toward predicting disease development and/or recovery after injury. While the research focuses on blood vessels, findings are expected to also apply to other soft tissues. Results will advance injury prevention strategies and provide a foundation for optimization of design for both interventional procedures and implantable biomaterials and devices. These experiments will inform computer models that predict damage-induced changes in vessel behavior. Finally, the research will further develop methods for characterizing soft tissue damage, including collagen hybridizing peptide to quantify collagen damage. This award reflects NSF's statutory mission and has been deemed worthy of support through evaluation using the Foundation's intellectual merit and broader impacts review criteria.