Relationship between hypertension, hypertrophy, and opening angle of zero-stress state of arteries following aortic constriction.
Examination of changes occurring in the zero-stress state of an organ provides a way to study cellular growth in the organ due to change of physical stresses. The zero-stress state of the aorta is not a tube. It is a sector with an opening angle that varies with the location on the aorta and changes with cellular remodeling. Blood vessel remodeling can be induced by imposing a constriction on the abdominal aorta by a metal clip (aortic banding), which causes an increase of blood pressure, hypertrophy of the aortic wall, and large change of opening angle. The correlation of the opening angle with the blood vessel wall thickness and blood pressure changes in rat's aorta due to aortic banding is presented in this report. The opening angle changes daily following the aortic banding. Blood pressure rises in vessels of the upper body, but that in the lower body decreases at first and then rises to an asymptotic value. Blood vessel wall thickness increases in rough proportion to blood pressure. Vessel diameter changes also. But the most dramatic is the course of change of the zero-stress state. Typically, the time to reach 50 percent of asymptotic hypertrophy of blood vessel wall thickness is about 3-5 days. The corresponding time for blood pressure is about 7 days. The opening angle of the zero-stress state, however, increases rapidly at first, reaches a peak in about 2 to 4 days, then decreases gradually to a reduced asymptote. The exact values of the time constants depend on the location along the aortic tree. In general, the course of change of residual strain is very different from those of the blood pressure and the blood vessel wall thickness.
Liu
S Q
SQ
Department of AMES/Bioengineering, University of California, San Diego, La Jolla 92093-0412.
Fung
Y C
YC
D000818:Animals; D001012:Aorta, Abdominal; D001018:Aortic Diseases / Q000473:pathology / Q000503:physiopathology*; D003251:Constriction, Pathologic / Q000473:pathology / Q000503:physiopathology; D003627:Data Interpretation, Statistical; D006439:Hemodynamics / Q000502:physiology; D006973:Hypertension / Q000503:physiopathology*; D006984:Hypertrophy; D051381:Rats; D011919:Rats, Inbred Strains; D013314:Stress, Mechanical