000011739 001__ 11739
000011739 005__ 20190219123652.0
000011739 037__ $$aTESIS-2013-074
000011739 041__ $$aeng
000011739 080__ $$a621
000011739 1001_ $$aSáez Viñas, Pablo
000011739 24500 $$aTheoretical and computational study of the mechano-biology in hypertension disease
000011739 260__ $$aZaragoza$$bUniversidad de Zaragoza, Prensas de la Universidad$$c2013
000011739 300__ $$a276
000011739 4900_ $$aTesis de la Universidad de Zaragoza$$v2013-56$$x2254-7606
000011739 500__ $$aPresentado: 08 07 2013
000011739 502__ $$aTesis-Univ. Zaragoza, Ingeniería Mecánica, 2013$$bZaragoza, Universidad de Zaragoza$$c2013
000011739 506__ $$aby-nc-nd$$bCreative Commons$$c3.0$$uhttps://creativecommons.org/licenses/by-nc-nd/3.0/
000011739 520__ $$aThe present work deals with the development of a theoretical and computational framework of the mechano-biology happening in the arterial tissue during hypertension disease. Biological tissue adapts actively to different mechanical and chemical stimuli where the underlying mechanical properties of the tissue play an important role. The mechanical stimuli that trigger these changes is the increase of blood pressure experienced in hypertensive patients. There are also changes in the blood flow. This work is divided in four aspects of the adaptation of different components of the tissue to hypertension. Firsts, we focus on the mechanical properties of the arterial tissue and we particularly look at the behavior of a real human carotid artery. We obtain a finite element model of the carotid artery to apply all the models developed during this work. Two of them are related with the growth and remodeling of the collagen and smooth muscle cells within the arterial wall. Its thermodynamic description fall into the description of open systems where mass is allowed to gain or loss via changes of volume, density of both. The characteristic thickening of the arterial wall is describe by means of a volumetric growth model. The stiffening of the arterial tissue, which is due to the increase of the collagen content, is formulated within a density growth model. Both of these approaches are described theoretically and are later included computationally in a finite element framework. The last part of this dissertation aims at deriving a model of endothelial cell orientation and morphological adaptation to the blood flow.
000011739 6531_ $$amechanical engineering
000011739 6531_ $$abioengineering
000011739 6531_ $$amecánica de medios continuos
000011739 6531_ $$abiomecánica
000011739 700__ $$aPeña Baquedano, Estefanía$$edir.
000011739 700__ $$aMartínez Barca, Miguel Ángel$$edir.
000011739 7102_ $$aUniversidad de Zaragoza$$bIngeniería Mecánica
000011739 8560_ $$fzaguan@unizar.es
000011739 8564_ $$s31861382$$uhttps://zaguan.unizar.es/record/11739/files/TESIS-2013-074.pdf$$zTexto completo (eng)
000011739 909CO $$ooai:zaguan.unizar.es:11739
000011739 909co $$ptesis
000011739 909CO $$pdriver
000011739 9102_ $$aIngeniería mecánica$$bIngeniería Mecánica
000011739 980__ $$aTESIS