Residual strain and local strain distributions in the rabbit atherosclerotic aorta.
Effect of atherosclerosis on the residual strain in the arterial wall was studied in the rabbit thoracic aorta. Atherosclerosis was induced by feeding a cholesterol diet or by combining denudation of aortic endothelial cells with the diet feeding. Diameter of each aorta in the physiological state was determined from a static pressure-diameter test. A ring specimen was obtained from the position where the diameter was measured. After the measurement of its no-load diameters, the ring was cut radially to measure the opening angle. Histological section was then obtained from the opened-up ring specimen. The section was divided into 32 subsections and local dimensions were measured for each subsection. Residual and in vivo strains referring to the opened-up configuration were calculated from the local dimensions and the diameters in the unloaded and physiological states. The opening angle significantly correlated with the area fraction of intimal hyperplasia until severe calcification occurred, while it had a negative correlation with the area fraction of calcified region. Histological observation of opened-up ring specimens indicated that the media adjacent to hyperplastic intima remained stretched, while that away from the intima relaxed. Analysis of local strains showed that, in the atherosclerotic aorta without calcification, higher residual strain (compressive), i.e., lower in vivo strain (tensile), appears in the thicker intima. These results suggest that: (a) intimal hyperplasia increases residual strain and thus reduces the in vivo strain exerted in the intima and (b) calcified tissue restrains the deformation of adjacent tissues. The intimal hyperplasia and the calcification may complicate strain fields in the atherosclerotic aorta.
Matsumoto
T
T
Department of Mechatronics and Precision Engineering, Faculty of Engineering, Tohoku University, Sendai, Japan.
Hayashi
K
K
Ide
K
K
D000818:Animals; D001011:Aorta / Q000473:pathology / Q000503:physiopathology*; D001161:Arteriosclerosis / Q000473:pathology / Q000503:physiopathology*; D001696:Biomechanical Phenomena; D008297:Male; D008955:Models, Cardiovascular; D011817:Rabbits; D013314:Stress, Mechanical