scholarly journals A Microstructurally Driven Model for Pulmonary Artery Tissue

2011 ◽  
Vol 133 (5) ◽  
Author(s):  
Philip H. Kao ◽  
Steven R. Lammers ◽  
Lian Tian ◽  
Kendall Hunter ◽  
Kurt R. Stenmark ◽  
...  

A new constitutive model for elastic, proximal pulmonary artery tissue is presented here, called the total crimped fiber model. This model is based on the material and microstructural properties of the two main, passive, load-bearing components of the artery wall, elastin, and collagen. Elastin matrix proteins are modeled with an orthotropic neo-Hookean material. High stretch behavior is governed by an orthotropic crimped fiber material modeled as a planar sinusoidal linear elastic beam, which represents collagen fiber deformations. Collagen-dependent artery orthotropy is defined by a structure tensor representing the effective orientation distribution of collagen fiber bundles. Therefore, every parameter of the total crimped fiber model is correlated with either a physiologic structure or geometry or is a mechanically measured material property of the composite tissue. Further, by incorporating elastin orthotropy, this model better represents the mechanics of arterial tissue deformation. These advancements result in a microstructural total crimped fiber model of pulmonary artery tissue mechanics, which demonstrates good quality of fit and flexibility for modeling varied mechanical behaviors encountered in disease states.

2014 ◽  
Vol 3 (2) ◽  
pp. 231-245 ◽  
Author(s):  
Sergei A. Avdonin ◽  
◽  
Boris P. Belinskiy ◽  

Author(s):  
Henry W. Haslach ◽  
Jonathan Chung ◽  
Aviva Molotsky

Rupture of vascular tissue in the circulatory system under non-impact loading is involved in potentially life threatening events such as Marfan’s syndrome or rupture of small renal veins during shock wave lithotripsy. The rupture mechanisms are not well-understood. The complexity of the artery wall precludes the use of rupture theories invented for metals or for fibered composites with a homogeneous matrix. Artery tissue is composed of ground material, smooth muscle cells, elastin and collagen. The collagen fibers, which are generally circumferentially oriented, are the load carrying material after large deformations. Clark and Glagov [1] propose that the media of an elastic artery is built of musculo-elastic fascicles made up of a layer of circumferentially oriented SMC that lie parallel and between two elastin lamellae. Between the elastin sheets of adjacent elements are interspersed collagen fiber bundles.


Author(s):  
Matthew D. Landrigan ◽  
Ryan K. Roeder

The accumulation of fatigue damage in bovine and human cortical bone is conventionally measured by modulus or stiffness degradation. The initial modulus or stiffness of each specimen is typically measured in order to normalize tissue heterogeneity to a prescribed strain [1,2]. Cyclic preloading at 100 N for 20 cycles has been used for this purpose in both uniaxial tension and four-point bending tests [1–3]. In four-point bending, the specimen modulus is often calculated using linear elastic beam theory as, (1)E=3Fl4bh2ε where F is the applied load, l is the outer support span, b is the specimen width, h is the specimen height, and ε is the maximum strain based on the beam deflection [2]. The maximum load and displacement data from preloading is used to determine the initial specimen modulus. The initial modulus and a prescribed maximum initial strain are then used to determine an appropriate load for fatigue testing under load control.


Author(s):  
Bahar Fata ◽  
Christopher A. Carruthers ◽  
Gregory A. Gibson ◽  
Simon C. Watkins ◽  
Danielle Gottlieb ◽  
...  

It has been estimated that worldwide 600,000 babies are born annually with significant congenital heart disease (1). Congenital heart and related vascular defects cause increased flow and pulmonary pressure leading to unfavorable vascular remodeling that results in pulmonary arterial hypertension (1). Developing tissue engineered replacements that mimic the growth and remodeling behavior of native tissue is the optimal approach in treatment of congenital arterial anomalies. The understanding of the underlying mechanisms leading to pulmonary arterial hypertension as well as replicating native pulmonary artery functionality in engineered replacements requires knowledge of native tissue mechanics and growth behavior. In the present study, we report novel information on the changes in the structure-mechanics behavior of the growing pulmonary artery.


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