Experimental investigation of the distribution of residual strains in the artery wall.
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.
Greenwald
S E
SE
Institute of Pathology, London Hospital Medical College, United Kingdom.
Moore
J E
JE
Rachev
A
A
Kane
T P
TP
Meister
J J
JJ
D000704:Analysis of Variance; D000818:Animals; D001012:Aorta, Abdominal / Q000473:pathology / Q000502:physiology; D001013:Aorta, Thoracic / Q000473:pathology / Q000502:physiology; D001158:Arteries / Q000473:pathology / Q000502:physiology*; D002339:Carotid Arteries / Q000473:pathology / Q000502:physiology; D002417:Cattle; D066298:In Vitro Techniques; D008297:Male; D008955:Models, Cardiovascular; D051381:Rats; D017207:Rats, Sprague-Dawley; D013314:Stress, Mechanical