Vascular Smooth Muscle and the Anisotropy of Dog Carotid Artery

Segments of dog carotid artery were held at in-situ length and studied in vitro after excitation of the muscle with norepinephrine and after poisoning of the muscle with potassium cyanide. In-situ length corresponded to a longitudinal strain of .57±.02 relative to the unstretched length. The longitudinal elastic modulus was about 4.1×106 dyn/cm2 at in-situ length and zero transmural pressure. This value was not altered by excitation of the vascular smooth muscle. The longitudinal stress due to traction decreased as the longitudinal stress due to transmural pressure increased, and it was suggested that this interaction underlies the relative constancy of vessel length in situ. The Poisson's ratio between the circumferential and longitudinal directions was about 0.3 and was found to decrease slightly with activation of the vascular muscle. The data for the longitudinal modulus and for Poisson's ratio were used to compute the circumferential elastic modulus. Activation of the muscle increased the circumferential elastic modulus when plotted as a function of circumferential strain. Comparison between the moduli in the two directions revealed that the arterial wall is not isotropic at physiological pressures because the circumferential elastic modulus is greater than the longitudinal modulus. Calculations indicated that assuming isotropy slightly underestimates the true circumferential modulus at small circumferential strains, and greatly overestimates the true circumferential modulus at large circumferential strains. Active smooth muscle has little direct effect on these estimations, but does alter the error by contracting the vessel to smaller strains.

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