Experimental Investigation of the Distribution of Residual Strains in the Artery Wall

Abstract

Arterial wall stresses are thought to be a major determinant of vascular remodeling both during normal growth and throughout the development of occlusive vascular disease. A completely physiologic mechanical model of the arterial wall should account not only for its residual strains but also for its structural nonhomogeneity. It is known that each layer of the artery wall possesses different mechanical properties, but the distribution of residual strain among the different mechanical components, and thus the true zero stress state, remain unknown. In this study, two different sets of experiments were carried out in order to determine the distribution of residual strains in artery walls, and thus the true zero stress state. In the first, collagen and elastin were selectively eliminated by chemical methods and smooth muscle cells were destroyed by freezing. Dissolving elastin provoked a decrease in the opening angle, while dissolving collagen and destroying smooth muscle cells had no effect. In the second, different wall layers of bovine carotid arteries were removed from the exterior or luminal surfaces by lathing or drilling frozen specimens, and then allowing the frozen material to thaw before measuring residual strain. Lathing material away from the outer surface caused the opening angle of the remaining inner layers to increase. Drilling material from the inside caused the opening angle of the remaining outer layers to decrease. Mechanical nonhomogeneity, including the distribution of residual strains, should thus be considered as an important factor in determining the distribution of stress in the artery wall and the configuration of the true zero stress state.

The three-dimensional micro- and nanostructure of the aortic medial lamellar unit measured using 3D confocal and electron microscopy imaging☆

“…Previous studies suggest that only 6-7% of collagen fibers are engaged at physiological pressure (Armentano et al, 1991;Greenwald et al, 1997). Our study visually confirmed that collagen fiber bundles were not taut at mean physiological pressure, and estimated a comparable recruitment of collagen fibers.…”

A model for arterial adaptation combining microstructural collagen remodeling and 3D tissue growth

“…In other words, the reference state for elastin (or natural state as called by Humphrey and Rajagopal) is the initial stress-free reference state and thus elastin is stretched in the unloaded (free of external loading) grown state, whereas collagen and smooth muscle cells are not. This implies that residual stress in the latter state is borne by elastin only, which is consistent with the observation by Greenwald et al (1997) on the role of elastin as a carrier of residual stress.…”

“…However, the latter conclusion is not in agreement with the observation by Greenwald et al (1997), that elastin plays a key role in the opening angle of arteries, whereas the other two mechanically important tissue components, smooth muscle cells and collagen, have no effect on the opening angle. This suggests that residual stress is linked to elastin only.…”

“…This suggests that residual stress is linked to elastin only. The observation by Greenwald et al (1997) fits in elegantly with the constrained mixture approach, proposed by Humphrey and Rajagopal (2002). In this approach, tissue components are assumed to be in a state of continuous turnover and new components can be created at a stress-free state that differs from that of the old components.…”

Evaluating the mechanical behavior of arterial tissue using digital image correlation

“…However, the tissue's mechanical response to axial loading is also influenced by the residual stress existing within the intimal and medial layers. 28,29 The arterial specimens have a natural curvature in the circumferential direction resulting from the residual stress that can contribute to defocusing and speckle decorrelation as well. The effect of defocus on strain errors was not considered.…”