The main hemodynamic forces acting on the vessel wall are the wall shear stress (WSS), caused by the friction of the flowing blood on the endothelial surface, and the circumferential stress caused by blood pressure, acting on endothelial cells and on smooth muscle cells. Experimental studies on the effects of disturbed flow contribute to our understanding of the pathophysiological mechanisms of vascular diseases, helping in ameliorating therapeutic interventions. The perivascular placement of a silastic collar around the carotid artery represents an established model of intimal thickening in rabbits and mice for testing mechanistic hypothesis on the pathogenesis of atherosclerosis and for assessment of anti-atherosclerotic interventions. In this work we adopted a one-way coupled, fluid-structure interaction approach to investigate the immediate fluid-dynamic alterations induced by perivascular collar placement on rabbit common carotid artery and establish a correlation between the early atherogenic events and the modifications of the hemodynamic environment. The results from this computational study help quantify the role of the local fluid-dynamics among the possible factors promoting the atherogenic processes in this experimental model. In particular, values of WSS and circumferential stress lower than in the physiological situation were found in the arterial region between the two collar-vessel contact points.

Fluid–Structure computational analysis to investigate the link between early atherogenic events and the hemodynamic environment in an experimental model of intimal thickening / E. Donetti, I. Decorato, E. Bertarelli, R. Baetta, A. Corsini, C. Sforza, G. Dubini. - In: CARDIOVASCULAR ENGINEERING AND TECHNOLOGY. - ISSN 1869-408X. - 3:3(2012 Sep), pp. 282-291. [10.1007/s13239-012-0100-z]

Fluid–Structure computational analysis to investigate the link between early atherogenic events and the hemodynamic environment in an experimental model of intimal thickening

E. Donetti
Primo
Conceptualization
;
R. Baetta;A. Corsini
Validation
;
C. Sforza
Penultimo
Methodology
;
2012

Abstract

The main hemodynamic forces acting on the vessel wall are the wall shear stress (WSS), caused by the friction of the flowing blood on the endothelial surface, and the circumferential stress caused by blood pressure, acting on endothelial cells and on smooth muscle cells. Experimental studies on the effects of disturbed flow contribute to our understanding of the pathophysiological mechanisms of vascular diseases, helping in ameliorating therapeutic interventions. The perivascular placement of a silastic collar around the carotid artery represents an established model of intimal thickening in rabbits and mice for testing mechanistic hypothesis on the pathogenesis of atherosclerosis and for assessment of anti-atherosclerotic interventions. In this work we adopted a one-way coupled, fluid-structure interaction approach to investigate the immediate fluid-dynamic alterations induced by perivascular collar placement on rabbit common carotid artery and establish a correlation between the early atherogenic events and the modifications of the hemodynamic environment. The results from this computational study help quantify the role of the local fluid-dynamics among the possible factors promoting the atherogenic processes in this experimental model. In particular, values of WSS and circumferential stress lower than in the physiological situation were found in the arterial region between the two collar-vessel contact points.
circumferential stress; common carotid artery; fluid-structure interaction; oscillatory shear index; wall shear stress
Settore BIO/16 - Anatomia Umana
Settore BIO/14 - Farmacologia
set-2012
Article (author)
File in questo prodotto:
File Dimensione Formato  
s13239-012-0100-z.pdf

accesso riservato

Tipologia: Publisher's version/PDF
Dimensione 668.94 kB
Formato Adobe PDF
668.94 kB Adobe PDF   Visualizza/Apri   Richiedi una copia
Pubblicazioni consigliate

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/195008
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 0
  • ???jsp.display-item.citation.isi??? ND
social impact