title: Stress and strain distribution in hypertensive and normotensive rat aorta considering residual strain.
abstract: The effects of hypertension on the stress and strain distributions through the wall thickness were studied in the rat thoracic aorta. Goldblatt hypertension was induced by constricting the left renal artery for 8 weeks. Static pressure-diameter-axial force relations were determined on excised tubular segments. The segments were then sliced into thin ring specimens. Circumferential strain distributions were determined from the cross-sectional shape of the ring specimens observed before and after releasing residual stresses by radial cutting. Stress distributions were calculated using a logarithmic type of strain energy density function. The wall thickness at the systolic blood pressure, P(sys) significantly correlated with P(sys). The mean stress and strain developed by P(sys) in the circumferential direction were not significantly different between the hypertensive and control aortas, while those in the axial direction were significantly smaller in the hypertensive aorta than in the control. The opening angles of the stress free ring specimens correlated well with P(sys). The stress concentration factor in the circumferential direction was almost constant and independent of P(sys) although the stress distributions were not uniform through the wall thickness. Histological observation showed that the wall thickening caused by hypertension is mainly due to the hypertrophy of the lamellar units of the media, especially in the subintimal layer where the stress increase developed by hypertension is larger than in the other layers. These results indicate that: (a) the aortic wall adapts itself to the mechanical field by changing not only the wall dimensions but also the residual stresses, (b) this adaptation is primarily related to the circumferential stress but not to the axial stress, and (c) the aortic smooth muscle cells seem to change their morphology in response to the mechanical stress.
authors.affiliation: Department of Mechatronics and Precision Engineering, Faculty of Engineering, Tohoku University, Sendai, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Matsumoto
authors.forename: K
authors.initials: K
authors.lastname: Hayashi
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D001013:Aorta, Thoracic / Q000473:pathology / Q000502:physiology / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000166:cytology / Q000473:pathology; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D008853:Microscopy; D008955:Models, Cardiovascular; D051381:Rats; D017208:Rats, Wistar; D013314:Stress, Mechanical; D013718:Tensile Strength