The stress analysis of vessel wall in the entrance region of a tapered vessel

1994 ◽  
Vol 15 (12) ◽  
pp. 1139-1147
Author(s):  
Cen Ren-jing ◽  
Tan Zhe-dong ◽  
Chen Zheng-zong
Author(s):  
Evelyne van Dam ◽  
Marcel Rutten ◽  
Frans van de Vosse

Rupture risk of abdominal aortic aneurysms (AAA) based on wall stress analysis may be superior to the currently used diameter-based rupture risk prediction [4; 5; 6; 7]. In patient specific computational models for wall stress analysis, the geometry of the aneurysm is obtained from CT or MR images. The wall thickness and mechanical properties are mostly assumed to be homogeneous. The pathological AAA vessel wall may contain collageneous areas, but also calcifications, cholesterol crystals and large amounts of fat cells. No research has yet focused yet on the differences in mechanical properties of the components present within the degrading AAA vessel wall.


1995 ◽  
Vol 16 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Cen Ren-jing ◽  
Qin Chan ◽  
Tan Zhe-dong

2020 ◽  
Vol 134 (17) ◽  
pp. 2399-2418
Author(s):  
Yoshito Yamashiro ◽  
Hiromi Yanagisawa

Abstract Blood vessels are constantly exposed to mechanical stimuli such as shear stress due to flow and pulsatile stretch. The extracellular matrix maintains the structural integrity of the vessel wall and coordinates with a dynamic mechanical environment to provide cues to initiate intracellular signaling pathway(s), thereby changing cellular behaviors and functions. However, the precise role of matrix–cell interactions involved in mechanotransduction during vascular homeostasis and disease development remains to be fully determined. In this review, we introduce hemodynamics forces in blood vessels and the initial sensors of mechanical stimuli, including cell–cell junctional molecules, G-protein-coupled receptors (GPCRs), multiple ion channels, and a variety of small GTPases. We then highlight the molecular mechanotransduction events in the vessel wall triggered by laminar shear stress (LSS) and disturbed shear stress (DSS) on vascular endothelial cells (ECs), and cyclic stretch in ECs and vascular smooth muscle cells (SMCs)—both of which activate several key transcription factors. Finally, we provide a recent overview of matrix–cell interactions and mechanotransduction centered on fibronectin in ECs and thrombospondin-1 in SMCs. The results of this review suggest that abnormal mechanical cues or altered responses to mechanical stimuli in EC and SMCs serve as the molecular basis of vascular diseases such as atherosclerosis, hypertension and aortic aneurysms. Collecting evidence and advancing knowledge on the mechanotransduction in the vessel wall can lead to a new direction of therapeutic interventions for vascular diseases.


1984 ◽  
Vol 45 (C1) ◽  
pp. C1-901-C1-904 ◽  
Author(s):  
C. Marinucci ◽  
L. Palladino ◽  
G. Pasotti ◽  
M. V. Ricci ◽  
G. Vécsey

2003 ◽  
Vol 100 (12) ◽  
pp. 1137-1149
Author(s):  
M. François

1999 ◽  
Vol 82 (S 01) ◽  
pp. 32-37 ◽  
Author(s):  
Karlheinz Peter ◽  
Wolfgang Kübler ◽  
Johannes Ruef ◽  
Thomas K. Nordt ◽  
Marschall S. Runge ◽  
...  

SummaryThe initiating event of atherogenesis is thought to be an injury to the vessel wall resulting in endothelial dysfunction. This is followed by key features of atherosclerotic plaque formation such as inflammatory responses, cell proliferation and remodeling of the vasculature, finally leading to vascular lesion formation, plaque rupture, thrombosis and tissue infarction. A causative relationship exists between these events and oxidative stress in the vessel wall. Besides leukocytes, vascular cells are a potent source of oxygen-derived free radicals. Oxidants exert mitogenic effects that are partially mediated through generation of growth factors. Mitogens, on the other hand, are potent stimulators of oxidant generation, indicating a putative self-perpetuating mechanism of atherogenesis. Oxidants influence the balance of the coagulation system towards platelet aggregation and thrombus formation. Therapeutic approaches by means of antioxidants are promising in both experimental and clinical designs. However, additional clinical trials are necessary to assess the role of antioxidants in cardiovascular disease.


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