Arterial Wall Mechanics in Conscious Dogs

Abstract

To evaluate arterial physiopathology, complete arterial wall mechanical characterization is necessary. This study presents a model for determining the elastic response of elastin (ς_E, where ς is stress), collagen (ς_C), and smooth muscle (ς_SM) fibers and viscous (ς_η) and inertial (ς_M) aortic wall behaviors. Our work assumes that the total stress developed by the wall to resist stretching is governed by the elastic modulus of elastin fibers (E_E), the elastic modulus of collagen (E_C) affected by the fraction of collagen fibers (f_C) recruited to support wall stress, and the elastic modulus of the maximally contracted vascular smooth muscle (E_SM) affected by an activation function (f_A). We constructed the constitutive equation of the aortic wall on the basis of three different hookean materials and two nonlinear functions, f_A and f_C: where ε is strain and ε_0E is strain at zero stress. Stress-strain relations in the control state and during activation of smooth muscle (phenylephrine, 5 μg · kg⁻¹ · min⁻¹ IV) were obtained by transient occlusions of the descending aorta and the inferior vena cava in 15 conscious dogs by using descending thoracic aortic pressure (microtransducer) and diameter (sonomicrometry) measurements. The f_C was not linear with strain, and at the onset of significant collagen participation in the elastic response (break point of the stress-strain relation), 6.02±2.6% collagen fibers were recruited at 23% of stretching of the unstressed diameter. The f_A exhibited a skewed unimodal curve with a maximum level of activation at 28.3±7.9% of stretching. The aortic wall dynamic behavior was modified by activation increasing viscous (η) and inertial (M) moduli from the control to active state (viscous, 3.8±1.3×10⁴ to 7.8±1.1×10⁴ dyne · s · cm⁻², P<.0005; inertial, 61±42 to 91±23 dyne · s² · cm⁻², P<.05). Finally, the purely elastic stress-strain relation was assessed by subtracting the viscous and inertial behaviors.