scholarly journals Aortic and Arterial Mechanics

2018 ◽  
pp. 183-226 ◽  
Author(s):  
S. Avril
Keyword(s):  
2021 ◽  
pp. 110856
Author(s):  
Ryan J. Pewowaruk ◽  
Omid Forouzan ◽  
Farhan Raza ◽  
Adam D. Gepner ◽  
Naomi C. Chesler

2017 ◽  
Vol 14 (136) ◽  
pp. 20170615 ◽  
Author(s):  
Michele Marino ◽  
Giuseppe Pontrelli ◽  
Giuseppe Vairo ◽  
Peter Wriggers

This paper presents a chemo-mechano-biological framework for arterial physiopathology. The model accounts for the fine remodelling in the multiscale hierarchical arrangement of tissue constituents and for the diffusion of molecular species involved in cell–cell signalling pathways. Effects in terms of alterations in arterial compliance are obtained. A simple instructive example is introduced. Although oversimplified with respect to realistic case studies, the proposed application mimics the biochemical activity of matrix metalloproteinases, transforming growth factors beta and interleukins on tissue remodelling. Effects of macrophage infiltration, of intimal thickening and of a healing phase are investigated, highlighting the corresponding influence on arterial compliance. The obtained results show that the present approach is able to capture changes in arterial mechanics as a consequence of the alterations in tissue biochemical environment and cellular activity, as well as to incorporate the protective role of both autoimmune responses and pharmacological treatments.


Author(s):  
Yanhang Zhang ◽  
Shahrokh Zeinali-Davarani
Keyword(s):  

2020 ◽  
Vol 201 (3) ◽  
pp. 371-374 ◽  
Author(s):  
Jennifer L. Philip ◽  
Diana M. Tabima ◽  
Gregory D. Wolf ◽  
Andrea L. Frump ◽  
Tik-Chee Cheng ◽  
...  

2004 ◽  
Vol 287 (4) ◽  
pp. L649-L655 ◽  
Author(s):  
Christa Boer ◽  
Geerten P. van Nieuw Amerongen ◽  
A. B. Johan Groeneveld ◽  
Gert Jan Scheffer ◽  
Jaap J. de Lange ◽  
...  

Endotoxemia is associated with changed pulmonary vascular function with respect to vasoreactivity, endothelial permeability, and activation of inducible nitric oxide synthase II (NOSII). However, whether altered passive arterial wall mechanics contribute to this endotoxin-induced pulmonary vascular dysfunction is still unknown. Therefore, we investigated whether endotoxin affects the passive arterial mechanics and compliance of isolated rat pulmonary arteries. Pulmonary arteries of pentobarbital-anesthetized Wistar rats ( n = 55) were isolated and exposed to Escherichia coli endotoxin (50 μg/ml) for 20 h. Endotoxin increased pulmonary artery diameter and compliance (transmural pressure = 13 mmHg) in an endothelium-, Ca2+-, or NOSII-induced NO release-independent manner. Interestingly, the endotoxin-induced alterations in the passive arterial mechanics were accompanied by disassembly of the smooth muscle cell (SMC) F-actin cytoskeleton. Disassembly of F-actin by incubation of control arteries with the cytoskeleton-disrupting agent cytochalasin B or the Rho-kinase inhibitor Y-27632 induced a similar increase in passive arterial diameter and compliance. In contrast, RhoA activation by lysophosphatidic acid prevented the endotoxin-induced alterations in the pulmonary SMC F-actin cytoskeleton and passive mechanics. In conclusion, these findings indicate that disassembly of the SMC F-actin cytoskeleton and RhoA/Rho-kinase signaling act as mediators of endotoxin-induced changes in the pulmonary arterial mechanics. They imply the involvement of F-actin rearrangement and RhoA/Rho-kinase signaling in endotoxemia-induced vascular lung injury.


2016 ◽  
Vol 248 ◽  
pp. 84-90 ◽  
Author(s):  
Sung-Ai Kim ◽  
Sun-Hee Park ◽  
Sang-Ho Jo ◽  
Kyoung-Ha Park ◽  
Hyun-Sook Kim ◽  
...  

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