Contribution of individual structural components in determining the zero-stress state in small arteries.
Arterial-wall stress distributions are important determinants of arterial function and are determined by the mechanical properties of the vessel wall, the physiological loading conditions, and the zero stress state of the artery. In this study, the relationship between this zero-stress state, the contractile state of the vessel, and the extracellular matrix components was investigated. Rat saphenous arteries were excised, and cross-sectional slices were cut. Wall thickness, intimal circumference, medial to adventitial border circumference, and the outer adventitial circumference were measured. Each slice was cut once longitudinally to relieve the residual stresses, and after a period of 30 min, vessel dimensions were again measured, and the angle to which the arterial section opened, a measure of the residual stress present in the intact artery, was recorded in this new zero-stress state. Control 'opening angle' was 112+/-10 degrees (mean+/-SD, n= 8) as compared to 138+/-6 degrees (n = 18) and 127+/-6 degrees (n = 11) for slices placed in 10(-4) M adenosine at 25 and 37 degrees C, respectively. Fluorescein isothiocyanate dextran was also injected intravenously in 8 animals to measure the homeostatic lumen diameter and wall thickness using intravital microscopy. Comparison of homeostatic strains calculated from these in situ dimensions to residual strains indicated that a given opening angle produced a radially uniform circumferential strain only for a specific level of tone. These results suggest that smooth muscle tone can acutely modify residual strain, possibly through interconnections with matrix components. Furthermore, selective elimination of matrix components by post-treatment of zero-stress slices with elastase or collagenase in 6 animals each increased the opening angle by 53 and 70%, respectively, suggesting that the extracellular matrix structure may regulate arterial strains in the long term.
Zeller
P J
PJ
Department of Biomedical Engineering, University of Virginia, Charlottesville 22908, USA.
Skalak
T C
TC
D000241:Adenosine / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000033:anatomy & histology* / Q000502:physiology*; D017364:Collagenases / Q000378:metabolism; D016326:Extracellular Matrix Proteins / Q000502:physiology; D005260:Female; D006706:Homeostasis; D009119:Muscle Contraction; D009131:Muscle, Smooth, Vascular / Q000502:physiology; D010196:Pancreatic Elastase / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013314:Stress, Mechanical; D014664:Vasodilation / Q000502:physiology
D016326:Extracellular Matrix Proteins; D010196:Pancreatic Elastase; D017364:Collagenases; D000241:Adenosine