Textile artificial muscles were developed using weaving to increase the force and knitting to amplify the strain.

This study suggests a method to compute the material parameters for arteries in vivo from clinically registered pressure-radius signals. The artery is modelled as a hyperelastic, incompressible, thin-walled cylinder and the membrane stresses are computed using a strain energy. The material parameters are determined in a minimisation process by tuning the membrane stress to the stress obtained by enforcing global equilibrium. In addition to the mechanical model, the study also suggests a preconditioning of the pressure-radius signal. The preconditioning computes an average pressure-radius cycle from all consecutive cycles in the registration and removes, or reduces, undesirable disturbances. The effect is a robust parameter identification that gives a unique solution. The proposed method is tested on clinical data from three human abdominal aortas and the results show that the material parameters from the proposed method do not differ significantly (p < 0.01) from the corresponding parameters obtained by averaging the result from consecutive cycles.

Chemical kinetics of smooth muscle contraction affect mechanical properties of organs that function under finite strains. In an effort to gain further insight into organ physiology, we formulate a mechanochemical finite strain model by considering the interaction between mechanical and biochemical components of cell function during activation. We propose a new constitutive framework and use a mechanochemical device that consists of two parallel elements: (i) spring for the cell stiffness; (ii) contractile element for the sarcomere. We use a multiplicative decomposition of cell elongation into filament contraction and cross-bridge deformation, and suggest that the free energy be a function of stretches, four variables (free unphosphorylated myosin, phosphorylated cross-bridges, phosphorylated and dephosphorylated cross-bridges attached to actin), chemical state variable driven by Ca2+-concentration, and temperature. The derived constitutive laws are thermodynamically consistent. Assuming isothermal conditions, we specialize the mechanical phase such that we recover the linear model of Yang et al. [2003a. The myogenic response in isolated rat cerebrovascular arteries: smooth muscle cell. Med. Eng. Phys. 25, 691-709]. The chemical phase is also specialized so that the linearized chemical evolution law leads to the four-state model of Hai and Murphy [1988. Cross-bridge phosphorylation and regulation of latch state in smooth muscle. Am. J. Physiol. 254, C99-C106]. One numerical example shows typical mechanochemical effects and the efficiency of the proposed approach. We discuss related parameter identification, and illustrate the dependence of muscle contraction (Ca2+-concentration) on active stress and related stretch. Mechanochemical models of this kind serve the mathematical basis for analyzing coupled processes such as the dependency of tissue properties on the chemical kinetics of smooth muscle.

The mechanical properties of the aorta affect cardiac function and are related to cardiovascular morbidity/mortality. This study was designed to evaluate the isotropic (mainly elastin, elastin(iso)) and anisotropic (mainly collagen, collagen(ani)) material parameters within the human aorta in vivo. Thirty healthy men and women in three different age categories (23-30, 41-54, and 67-72 yr) were included. A novel mechanical model was used to identify the mechanical properties and the strain field with aid of simultaneously recorded pressure and radius in the abdominal aorta. The magnitudes of the material parameters relating to both the stiffness of elastin(iso) and collagen(ani) were in agreement with earlier in vitro studies. The load-bearing fraction attributed to collagen(ani) oscillated from 10 to 30% between diastolic and systolic pressures during the cardiac cycle. With age, stiffness of elastin(iso) increased in men, despite the decrease in elastin content that has been found due to elastolysis. Furthermore, an increase in stiffness of collagen(ani) at high physiological pressure was found. This might be due to increased glycation, as well as changed isoforms of collagen in the aortic wall with age. A marked sex difference was observed, with a much less age-related effect, both on elastin(iso) and collagen(ani) stiffness in women. Possible factors of importance could be the effect of sex hormones, as well as differing collagen isoforms, between the sexes.

This paper presents a modelling framework in which the mechanochemical properties of smooth muscle cells may be studied. The activation of smooth muscles is considered in a three-dimensional continuum model which is key to realistically capture the function of hollow organs such as blood vessels. On the basis of a general thermodynamical framework the mechanical and chemical phases are specialized in order to quantify the coupled mechanochemical process. A free-energy function is proposed as the sum of a mechanical energy stored in the passive tissue, a coupling between the mechanical and chemical kinetics and an energy related purely to the chemical kinetics and the calcium ion concentration. For the chemical phase it is shown that the cross-bridge model of Hai and Murphy (Am. J. Physiol. Cell Physiol., 254, C99-C106, 1988) is included in the developed evolution law as a special case. In order to show the specific features and the potential of the proposed continuum model a uniaxial extension test of a tissue strip is analysed in detail and the related kinematics and stress-stretch relations are derived. Parameter studies point to coupling phenomena; in particular the tissue response is analysed in terms of the calcium ion level. The model for smooth muscle contraction may significantly contribute to current modelling efforts of smooth muscle tissue responses.